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Post-concussion syndrome
|Post-concussion syndrome
|Other names: Postconcussive syndrome
|a,b) Significantly increased mean diffusivity in association with the severity of post-concussive symptoms
|Psychiatry, Neurology, physical medicine and rehabilitation
Post-concussion syndrome (PCS) is a set of symptoms that may continue for weeks, months, or a year or more after a concussion – a mild traumatic brain injury (TBI).[1][2][3] About 15–30% of people with concussion develop persistent or prolonged symptoms associated with the injury.[medical citation needed] Prolonged concussion is defined as having concussion symptoms for over four weeks following the first accident in youth and for weeks or months in adults.[4]
A diagnosis may be made when symptoms resulting from concussion last for more than three months after the injury.[5][6][needs update] Loss of consciousness is not required for a diagnosis of concussion or post-concussion syndrome.[7]
Though there is no specific treatment for PCS, symptoms can be improved with medications and physical and behavioral therapy. Education about symptoms and details about expectation of recovery are important. The majority of PCS cases resolve after a period of time.
Signs and symptoms
In the past, the term PCS was also used to refer to immediate physical symptoms or post-concussive symptoms following a minor TBI or concussion.[8] The severity of these symptoms typically decreases rapidly.[9] In addition, the nature of the symptoms may change over time: acute symptoms are most commonly of a physical nature, while persisting symptoms tend to be predominantly psychological.[10][11] Symptoms such as noise sensitivity, problems with concentration and memory, irritability, depression, and anxiety may be called 'late symptoms' because they generally do not occur immediately after the injury, but rather in the days or weeks after the injury.[8] Nausea and drowsiness commonly occur acutely following concussion. Headache and dizziness occur immediately after the injury, but also can be long lasting.[8]
The condition is associated with a wide range of non-specific symptoms: physical, such as headache; cognitive, such as difficulty concentrating; and emotional and behavioral, such as irritability. Many of the symptoms associated with PCS are common or may be exacerbated by other disorders, so there is considerable risk of misdiagnosis. Headaches that occur after a concussion may feel like migraine headaches or tension-type headaches. Most headaches are tension-type headaches, which may be associated with a neck injury that occurred at the same time of the head injury.[12][needs update]
A common condition associated with PCS is headache.[13][needs update] While most people have headaches of the same type they experienced before the injury, people diagnosed with PCS often report more frequent or longer-lasting headaches.[13] Between 30% and 90% of people treated for PCS report having more frequent headaches and between 8% and 32% still report them a year after the injury.[13][needs update]
Dizziness is another common symptom reported in about half of people diagnosed with PCS and is still present in up to a quarter of them a year after the injury.[13] Older people are at especially high risk for dizziness, which can contribute to subsequent injuries and higher rates of mortality due to falls.[14]
About 10% of people with PCS develop sensitivity to light or noise, about 5% experience a decreased sense of taste or smell, and about 14% report blurred vision.[13] People may also have double vision or ringing in the ears, also called tinnitus.[15] PCS may cause insomnia, fatigue,[16] or other problems with sleep.[9]
Psychological and behavioral
Psychological conditions, which are present in about half of people with PCS, may include irritability, anxiety, depression, and a change in personality.[13] Other emotional and behavioral symptoms include restlessness,[17] aggression,[18] and mood swings.[16][19] Some common symptoms, such as apathy, insomnia, irritability, or lack of motivation, may result from other co-occurring conditions, such as depression.[13]
Higher mental functions
Common symptoms associated with a diagnosis of PCS are related to cognition,[20] attention,[21] and memory, especially short-term memory, which can also worsen other problems such as forgetting appointments or difficulties at work.[13] In one study, one in four people diagnosed with PCS continued to report memory problems a year after the injury,[13][22] but most experts agree that cognitive symptoms clear within six months to a year after injury in the vast majority of individuals.[13][needs update]
The question of the cause or causes of PCS has been heavily debated for many years and remain controversial.[medical citation needed] It is not known to exactly what degree the symptoms are due to physiological changes or to other factors, such as pre-existing psychiatric disorders or factors related to secondary gain or disability compensation.[23] The subjectivity of the complaints complicates assessment and makes it difficult to determine whether symptoms are being exaggerated or feigned.[13]
PCS may also be exacerbated by psychosocial factors, chronic pain, or an interaction of some or all of these.[24] The majority of experts believe that PCS results from a mix of factors, including preexisting psychological factors and those directly relating to the physical injury.[8]
It is not known what causes PCS to occur and persist,[25] or why some people who suffer a mild traumatic brain injury later develop PCS while others do not.[26][needs update] The nature of the syndrome and the diagnosis itself have been the subject of intense debate since the 19th century. However, certain risk factors have been identified; for example, preexisting medical or psychological conditions, expectations of disability, being female, and older age all increase the chances that someone will suffer PCS. Physiological and psychological factors present before, during, and after the injury are all thought to be involved in the development of PCS.[8][needs update]
Some experts believe post-concussion symptoms are caused by structural damage to the brain or disruption of neurotransmitter systems, resulting from the impact that caused the concussion.[medical citation needed] Others believe that post-concussion symptoms are related to common psychological factors. Most common symptoms like headache, dizziness, and sleep problems are similar to those often experienced by individuals diagnosed with depression, anxiety, or post traumatic stress disorder.[medical citation needed] In many cases, both physiological effects of brain trauma and emotional reactions to these events play a role in the development of symptoms.[27]
Conventional neuroimaging studies of the brain following a concussion are typically normal. However, studies have found some subtle physiological changes associated with PCS using more novel imaging modalities.[medical citation needed] Studies using positron emission tomography have linked PCS to a reduction in glucose use by the brain.[medical citation needed] Changes in cerebral blood flow have also been observed as long as three years after a concussion in studies using single photon emission computed tomography (SPECT).[13][needs update] At least one study with functional magnetic resonance imaging (fMRI) has shown differences in brain function during tasks involving memory after mild traumatic brain injury (mTBI) although they were not examining PCS specifically.[28]
Not all people with PCS have abnormalities on imaging, however, and abnormalities found in studies such as fMRI, PET, and SPECT could result from other comorbid conditions such as depression, chronic pain, or posttraumatic stress disorder (PTSD).[24] Proponents of the view that PCS has a physiological basis point to findings that children demonstrate deficits on standardized tests of cognitive function following a mild TBI.[29] A few studies have shown that people with PCS score lower than controls on neuropsychological tests that measure attention, verbal learning, reasoning, and information processing, but issues related to effort and secondary gain can not be ruled out as contributing to these differences.[8] Recovery as measured by scores on cognitive tests frequently do not correlate with resolution of symptoms; individuals diagnosed with PCS may still report subjective symptoms after their performance on tests of cognitive functioning have returned to normal.[30] Another study found that although children with PCS had poorer scores on tests of cognitive functioning after the injury, they also had poorer behavioral adjustment before the injury than children with no persistent symptoms; these findings support the idea that PCS may result from a combination of factors such as brain dysfunction resulting from head injury and preexisting psychological or social problems.[29] Different symptoms may be predicted by different factors; for example, one study found that cognitive and physical symptoms were not predicted by the manner in which parents and family members coped with the injury and adjusted to its effects, but psychological and behavioral symptoms were.[29]
Brain inflammation is suggested to play a role in post-concussive syndrome.[31]
It has been argued that psychological factors play an important role in the presence of post-concussion symptoms.[32] The development of PCS may be due to a combination of factors such as adjustment to effects of the injury, preexisting vulnerabilities, and brain dysfunction.[33] Setbacks related to the injury, for example problems at work or with physical or social functioning, may act as stressors that interact with preexisting factors such as personality and mental conditions to cause and perpetuate PCS.[24] In one study, levels of daily stress were found to be correlated to PCS symptoms in both concussed subjects and controls, but in another, stress was not significantly related to symptoms.[8]
Iatrogenic effects (those caused by the medical intervention) may also occur when individuals are provided with misleading or incorrect information related to recovery of symptoms. This information may cause people to focus and dwell on the idea that their brains are permanently damaged,.[24] It appears that even the expectation of symptoms may contribute to the development of PCS by causing individuals with mTBI to focus on symptoms and therefore perceive them to be more intense, to attribute symptoms that occur for other reasons to the injury, and to underestimate the rate of symptoms before the injury.[30]
|Sleep problems
|Problems tolerating
|Affect changes,
anxiety, or depression
|Changes in
The International Statistical Classification of Diseases and Related Health Problems (ICD-10) and the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders have set out criteria for post-concussion syndrome (PCS) and post-concussional disorder (PCD), respectively.
The ICD-10 established a set of diagnostic criteria for PCS in 1992.[34] In order to meet these criteria, a patient has had a head injury "usually sufficiently severe to result in loss of consciousness"[29][35] and then develop at least three of the eight symptoms marked with a check mark in the table at right under "ICD-10" within four weeks.[34][36] About 38% of people who suffer a head injury with symptoms of concussion and no radiological evidence of brain lesions meet these criteria.[37] In addition to these symptoms, people that meet the ICD-10 criteria for PCS may fear that they will have permanent brain damage, which may worsen the original symptoms.[3] Preoccupation with the injury may be accompanied by the assumption of a "sick role" and hypochondriasis.[33] The criteria focus on subjective symptoms and mention that neuropsychological evidence of significant impairment is not present.[38] With their focus on psychological factors, the ICD-10 criteria support the idea that the cause of PCS is functional.[29] Like the ICD-10, the ICD-9-CM defines PCS in terms of subjective symptoms and discusses the greater frequency of PCS in people with histories of mental disorders or a financial incentive for a diagnosis.[38]
The DSM-IV lists criteria for diagnosis of PCD in people who have suffered a head trauma with persistent post-traumatic amnesia, loss of consciousness, or post-traumatic seizures.[29] In addition, for a diagnosis of PCD, patients must have neuropsychological impairment as well as at least three of the symptoms marked with a check mark in the table at right under "DSM-IV".[29] These symptoms must be present for three months after the injury and must have been absent or less severe before the injury.[39] In addition, the patient must experience social problems as a result, and must not meet criteria for another disorder that explains the symptoms better.[39]
Neuropsychological tests exist to measure deficits in cognitive functioning that can result from PCS.[13][22] The Stroop Color Test and the 2&7 Processing Speed Test (which both detect deficits in speed of mental processing) can predict the development of cognitive problems from PCS.[13] A test called the Rivermead Postconcussion Symptoms Questionnaire, a set of questions that measure the severity of 16 different post-concussion symptoms, can be self-administered or administered by an interviewer.[3] Other tests that can predict the development of PCS include the Hopkins Verbal Learning A test (HVLA) and the Digit Span Forward examination.[13] The HVLA tests verbal learning and memory by presenting a series of words and assigning points based on the number recalled,[40] and digit span measures attention efficiency by asking the examinee to repeat back digits spoken by the tester in the same order as they are presented.[41] In addition, neuropsychological tests may be performed to detect malingering (exaggerating or making up symptoms) .[9]
Differential diagnosis
PCS, which shares symptoms with a variety of other conditions, is highly likely to be misdiagnosed in people with these conditions.[42][needs update] Cognitive and affective symptoms that occur following a traumatic injury may be attributed to mTBI, but in fact be due to another factor such as posttraumatic stress disorder,[32] which is easily misdiagnosed as PCS and vice versa.[42] Affective disorders such as depression have some symptoms that can mimic those of PCS and lead to a wrongful diagnosis of the latter; these include problems with concentration, emotional lability, anxiety, and sleep problems.[13] Depression, which is highly common in persistent PCS, can worsen other PCS symptoms, such as headaches and problems with concentration, memory, and sleep.[43] PCS also shares symptoms with chronic fatigue syndrome, fibromyalgia, and exposure to certain toxins.[16] Traumatic brain injury may cause damage to the hypothalamus or the pituitary gland, and deficiencies of pituitary hormones (hypopituitarism) can cause similar symptoms to post-concussion syndrome; in these cases, symptoms can be treated by replacing any hormones that are deficient.[medical citation needed]
Management of post-concussion syndrome typically involves treatments addressing specific symptoms;[11] for example, people can take over the counter pain relievers for headaches and medicine to relieve depression or insomnia.[44][needs update] Participation in low-risk physical activities that raise the heart rate and mental activities is advised, at a level that does not worsen symptoms.[45] Prolonged rest is not suggested.[45] Physical and behavioral therapy may also be prescribed for problems such as loss of balance and difficulties with attention, respectively.[46]
Though no pharmacological treatments exist for PCS, doctors may prescribe medications used for symptoms that also occur in other conditions; for example, antidepressants are used for the depression that frequently follows mTBI.[47] Side effects of medications may affect people suffering the consequences of mTBI more severely than they do others, and thus it is recommended that medications be avoided if possible;[47] there may be a benefit to avoiding narcotic medications.[48] In addition, some pain medications prescribed for headaches can cause rebound headaches when they are discontinued.[49]
Psychological treatment, to which about 40% of PCS patients are referred for consultation,[37] has been shown to reduce problems.[3] Ongoing disabilities may be treated with therapy to improve function at work, or in social or other contexts. Therapy aims to aid in the gradual return to work and other preinjury activities, as symptoms permit. A protocol for PCS treatment has been designed based on the principles behind Cognitive behavioral therapy (CBT), a psychotherapy aimed at influencing disturbed emotions by improving thoughts and behaviors.[24] CBT may help prevent persistence of iatrogenic symptoms[47] – those that occur because health care providers create the expectation that they will. A risk exists that the power of suggestion may worsen symptoms and cause long-term disabilities;[49] therefore, when counseling is indicated, the therapist must take a psychological origin of symptoms into account and not assume that all symptoms are a direct result of neurological damage from the injury.[50]
In situations such as motor vehicle accidents or following a violent attack, the post-concussion syndrome may be accompanied by posttraumatic stress disorder, which is important to recognize and treat in its own right. People with PTSD, depression, and anxiety can be treated with medication and psychotherapy.[47]
Upper cervical care
Post-concussion syndrome can sometimes be the result of a misalignment in the upper cervical spine (neck) specifically the C1 (Atlas) or C2 (Axis) which surround the brain stem. Some individuals have found relief through upper cervical care. An upper cervical chiropractor is a specialist who uses x-rays to identify misalignments in the upper cervical spine then gently repositions the top two bones of the neck. There are currently approximately seven different chiropractic methods of repositioning the C1 bone, however the three most popular techniques are NUCCA (adjustment done by hand), Blair Technique (adjustment done by hand), and Atlas Orthogonal (adjustment done by a machine). [51]
Education about symptoms and their usual time course is a part of psychological therapy, and is most effective when provided soon after the injury.[47] Since stress exacerbates post-concussion symptoms, and vice versa, an important part of treatment is reassurance that PCS symptoms are normal, and education about how to deal with impairments.[17] One study found that PCS patients who were coached to return to activities gradually, told what symptoms to expect, and trained how to manage them had a reduction in symptoms compared to a control group of uninjured people.[10] Early education has been found to reduce symptoms in children as well.[46]
Neurotherapy is an operant conditioning test where patients are given conditional audio/visual rewards after producing particular types of brainwave activity. Recent neurotherapy improvements in quantitative electroencephalography can identify the specific brainwave patterns that need to be corrected. Studies have shown that neurotherapy is effective in the treatment of post-concussion syndrome and other disorders with similar symptoms.[52]
The prognosis for PCS is generally considered positive, with total resolution of symptoms in many, but not all, cases. For 50% of people, post-concussion symptoms go away within a few days to several weeks after the original injury occurs.[23] In others, symptoms may remain for three to six months,[20] but evidence indicates that many cases are completely resolved within six months.[13] The majority of symptoms are largely gone in about half of people with concussion one month after the injury, and about two thirds of people with minor head trauma are nearly symptom-free within three months. Persistent, often severe headaches are the longest lingering symptom in most cases and are the most likely symptom to never fully resolve.[47] It is frequently stated in the literature and considered to be common knowledge that 15–30% of people with PCS have not recovered by a year after the injury, but this estimate is imprecise because it is based on studies of people admitted to a hospital, the methodologies of which have been criticized.[24][42][53] In approximately 15% of people, symptoms may persist for years or be permanent. If symptoms are not resolved by one year, they are likely to be permanent, though improvements may occur after even two or three years,[39] or may suddenly occur after a long time without much improvement.[54] Older people and those who have previously suffered another head injury are likely to take longer to recover.[54]
The way in which children cope with the injury after it occurs may have more of an impact than factors that existed prior to the injury.[29] Children's mechanisms for dealing with their injuries may have an effect on the duration of symptoms, and parents who do not deal effectively with anxiety about children's post-injury functioning may be less able to help their children recover.[29]
If another blow to the head occurs after a concussion but before its symptoms have gone away, there is a slight risk of developing the serious second-impact syndrome (SIS).[55][56] In SIS, the brain rapidly swells, greatly increasing intracranial pressure.[55] People who have repeated mild head injuries over a prolonged period, such as boxers and Gridiron football players, are at risk for chronic traumatic encephalopathy (or the related variant dementia pugilistica), a severe, chronic disorder involving a decline in mental and physical abilities.[57]
It is not known exactly how common PCS is. Estimates of the prevalence at three months post-injury are between 24 and 84%, a variation possibly caused by different populations or study methodologies.[8][needs update] The estimated incidence of PPCS (persistent postconcussive syndrome) is around 10% of mTBI cases.[38] Since PCS by definition only exists in people who have suffered a head injury, demographics and risk factors are similar to those for head injury; for example, young adults are at higher risk than others for receiving head injury, and, consequently, of developing PCS.[39]
The existence of PCS in children is controversial. It is possible that children's brains have enough plasticity that they are not affected by long-term consequences of concussion (though such consequences are known to result from moderate and severe head trauma).[58] On the other hand, children's brains may be more vulnerable to the injury, since they are still developing and have fewer skills that can compensate for deficits.[59] Clinical research has found higher rates of post-concussion symptoms in children with TBI than in those with injuries to other parts of the body, and that the symptoms are more common in anxious children.[33] Symptoms in children are similar to those in adults, but children exhibit fewer of them.[33] Evidence from clinical studies found that high school-aged athletes had slower recoveries from concussion as measured by neuropsychological tests than college-aged ones and adults.[59] PCS is rare in young children.[48]
Risk factors
A wide range of factors have been identified as being predictive of PCS, including low socioeconomic status, previous mTBI, a serious associated injury, headaches, an ongoing court case, age and female sex.[50][60] Being older than 40 and being female have also been identified as being predictive of a diagnosis of PCS,[8] and women tend to report more severe symptoms.[13] In addition, the development of PCS can be predicted by having a history of alcohol use disorder, low cognitive abilities before the injury, a personality disorder, or a medical illness not related to the injury.[13] PCS is also more prevalent in people with a history of psychiatric conditions such as clinical depression or anxiety before the injury.[61][62][63]
Mild brain injury-related factors that increase the risk for persisting post-concussion symptoms include an injury associated with acute headache, dizziness, or nausea; an acute Glasgow Coma Score of 13 or 14; and suffering another head injury before recovering from the first.[11] The risk for developing PCS also appears to be increased in people who have traumatic memories of the injury or expect to be disabled by the injury.[11]
The symptoms that occur after a concussion have been described in various reports and writings for hundreds of years.[20] The idea that this set of symptoms forms a distinct entity began to attain greater recognition in the latter part of the 19th century.[64] John Erichsen, a surgeon from London, played an important role in developing the study of PCS.[64] The controversy surrounding the cause of PCS began in 1866 when Erichsen published a paper about persisting symptoms after sustaining mild head trauma.[13] He suggested that the condition was due to "molecular disarrangement" to the spine. The condition was originally called "railroad spine" because most of the injuries studied had happened to railroad workers.[13] While some of his contemporaries agreed that the syndrome had an organic basis, others attributed the symptoms to psychological factors or to outright feigning.[64] In 1879, the idea that a physical problem was responsible for the symptoms was challenged by Rigler, who suggested that the cause of the persisting symptoms was actually "compensation neurosis": the railroad's practice of compensating workers who had been injured was bringing about the complaints.[13] Later, the idea that hysteria was responsible for the symptoms after a mild head injury was suggested by Charcot.[13][65] Controversy about the syndrome continued through the 20th century.[65] During World War I many soldiers suffered from puzzling symptoms after being close to a detonation but without any evidence of a head wound. The illness was called shell shock, and a psychological explanation was eventually favoured.[66] By 1934 the current concept of PCS had replaced ideas of hysteria as the cause of post-concussion symptoms.[13] British authorities banned the term shell shock during World War II to avoid an epidemic of cases, and the term posttrauma concussion state was coined in 1939 to describe "disturbance of consciousness with no immediate or obvious pathologic change in the brain".[66] The term postconcussion syndrome was in use by 1941.[66]
In 1961, H. Miller first used the term "accident neurosis" to refer to the syndrome which is now called PCS and asserted that the condition only occurs in situations where people stand to be compensated for the injury.[30] The real causes of the condition remain unclear.[13]
Though no universally accepted definition of postconcussive syndrome exists, most of the literature defines the syndrome as the development of at least three of the following symptoms: headache, dizziness, fatigue, irritability, impaired memory and concentration, insomnia, and lowered tolerance for noise and light.[39] One complication in diagnosis is that symptoms of PCS also occur in people who have no history of head injury, but who have other medical and psychological complaints.[24] In one study 64% of people with TBI, 11% of those with brain injuries, and 7% of those with other injuries met the DSM-IV criteria for post-concussion syndrome. Many of these PCS sufferers were misdiagnosed as having other unrelated conditions due to commonality of symptoms. (see diagnosis above).[67]
Headache is one of the criteria for PCS, but it is notably undetermined where the headache comes from. Couch, Lipton, Stewart and Scher (2007)[68] argue that headaches, one of the hallmarks of PCS, occur in a variety of injuries to the head and neck. Further, Lew et al. (2006)[69] reviewed ample studies comparing headaches to post-traumatic headaches and found that there is wide heterogeneity in the source and causes of headaches. They point out that the International Headache Society lists 14 known causes of headaches, as well. Furthermore, the headaches may be better accounted for by mechanical causes, such as whiplash, which is often mistaken for PCS.[70] An additional possibility is that posttraumatic stress disorder can account for some cases diagnosed as PCS,[71] but for emotional regulation as well.[67][72]
Depression, posttraumatic stress disorder, and chronic pain share symptoms resembling those of PCS.[24] One study found that while people with chronic pain without TBI do report many symptoms similar to those of post-concussion syndrome, they report fewer symptoms related to memory, slowed thinking, and sensitivity to noise and light than people with mTBI do.[8] Additionally, it has been found that neuroendocrinology may account for depressive symptoms and stress management due to irregularities in cortisol regulation, and thyroid hormone regulation.[73] Lastly, there is evidence that major depression following TBI is quite common, but may be better accounted for with a diagnosis of dysexecutive syndrome.[74]
In a syndrome, a set of symptoms is consistently present, and symptoms are linked such that the presence of one symptom suggests that of others. Because PCS symptoms are so varied and many can be associated with a large number of other conditions, doubt exists about whether the term "syndrome" is appropriate for the constellation of symptoms found after concussion.[75] The fact that the persistence of one symptom is not necessarily linked to that of another has similarly led to doubt about whether "syndrome" is the appropriate term.[47]
A longstanding controversy surrounding PCS concerns the nature of its etiology – that is, the cause behind it[29] – and the degree to which psychological factors and organic factors involving brain dysfunction are responsible. The debate has been referred to as 'psychogenesis versus physiogenesis' (psychogenesis referring to a psychological origin for the condition, physiogenesis to a physical one).[29]
See also
- Daniel Amen, post-concussion expert for the National Football League
- ↑ "Post-concussion syndrome – Symptoms and causes". mayoclinic.com. Archived from the original on 2014-01-02. Retrieved 2022-04-16.
- ↑ Rao V, Lyketsos C (2000). "Neuropsychiatric sequelae of traumatic brain injury". Psychosomatics. 41 (2): 95–103. doi:10.1176/appi.psy.41.2.95. PMID 10749946.
- ↑ 3.0 3.1 3.2 3.3 Mittenberg W, Strauman S (2000). "Diagnosis of mild head injury and the postconcussion syndrome". Journal of Head Trauma Rehabilitation. 15 (2): 783–91. doi:10.1097/00001199-200004000-00003. PMID 10739967.
- ↑ Ontario Neurotrauma Foundation. "Guidelines for Concussion/mTBI and Persistent Symptoms: 3rd Ed". braininjuryguidelines.org. Archived from the original on 2021-06-08. Retrieved 2021-11-09.
- ↑ McHugh T, Laforce R, Gallagher P, Quinn S, Diggle P, Buchanan L (2006). "Natural history of the long-term cognitive, affective, and physical sequelae of a minor traumatic brain injury". Brain and Cognition. 60 (2): 209–11. doi:10.1016/j.bandc.2004.09.018. PMID 16646125. S2CID 53190838.
- ↑ Bigler ED (2008). "Neuropsychology and clinical neuroscience of persistent post-concussive syndrome". Journal of the International Neuropsychological Society. 14 (1): 1–22. doi:10.1017/S135561770808017X. PMID 18078527.
- ↑ "Post-concussion syndrome – Symptoms and causes". mayoclinic.org. Archived from the original on 2017-07-16. Retrieved 2022-04-16.
- ↑ 8.0 8.1 8.2 8.3 8.4 8.5 8.6 8.7 8.8 8.9 Ryan LM, Warden DL (2003). "Post concussion syndrome". International Review of Psychiatry. 15 (4): 310–16. doi:10.1080/09540260310001606692. PMID 15276952. S2CID 32790756. Archived from the original on 2019-12-10. Retrieved 2022-04-16.
- ↑ 9.0 9.1 9.2 Kushner D (1998). "Mild traumatic brain injury: Toward understanding manifestations and treatment". Archives of Internal Medicine. 158 (15): 1617–24. doi:10.1001/archinte.158.15.1617. PMID 9701095.
- ↑ 10.0 10.1 Weight DG (1998). "Minor head trauma". Psychiatric Clinics of North America. 21 (3): 609–24. doi:10.1016/S0193-953X(05)70026-5. PMID 9774799.
- ↑ 11.0 11.1 11.2 11.3 Anderson T, Heitger M, Macleod AD (2006). "Concussion and mild head injury". Practical Neurology. 6 (6): 342–57. doi:10.1136/jnnp.2006.106583. S2CID 73308864. Archived from the original on 2009-04-27. Retrieved 2022-04-16.
- ↑ "Post-concussion syndrome – Symptoms and causes". Mayo Clinic. Archived from the original on 2017-07-26. Retrieved 2022-04-16.
- ↑ 13.00 13.01 13.02 13.03 13.04 13.05 13.06 13.07 13.08 13.09 13.10 13.11 13.12 13.13 13.14 13.15 13.16 13.17 13.18 13.19 13.20 13.21 13.22 13.23 13.24 Hall RC, Hall RC, Chapman MJ (2005). "Definition, diagnosis, and forensic implications of postconcussional syndrome". Psychosomatics. 46 (3): 195–202. doi:10.1176/appi.psy.46.3.195. PMID 15883140. Archived from the original on 2005-05-15.
- ↑ Maskell F, Chiarelli P, Isles R (2006). "Dizziness after traumatic brain injury: overview and measurement in the clinical setting". Brain Inj. 20 (3): 293–305. doi:10.1080/02699050500488041. PMID 16537271. S2CID 34746334.
- ↑ Barth JT, Ruff R, Espe-Pfeifer P (2006). "Mild traumatic brain injury: Definitions". In Nicholson, Keith, Young, Gerald, Andrew K. Kane (eds.). Psychological Knowledge in Court: PTSD, Pain and TBI. Berlin: Springer. pp. 271–77. ISBN 0-387-25609-1.
- ↑ 16.0 16.1 16.2 Margulies S (September 2000). "The postconcussion syndrome after mild head trauma: Is brain damage overdiagnosed? Part 1". Journal of Clinical Neuroscience. 7 (5): 400–08. doi:10.1054/jocn.1999.0681. PMID 10942660. S2CID 38741663.
- ↑ 17.0 17.1 King NS. 2003. Post-concussion syndrome: clarity amid the controversy? Archived December 10, 2005, at the Wayback Machine. Accessed January 1, 2007.
- ↑ Shaw NA (2002). "The neurophysiology of concussion". Progress in Neurobiology. 67 (4): 281–344. doi:10.1016/S0301-0082(02)00018-7. PMID 12207973. S2CID 46514293.
- ↑ Jagoda A, Riggio S (2000). "Mild traumatic brain injury and the postconcussive syndrome". Emergency Medicine Clinics of North America. 18 (2): 355–363. doi:10.1016/S0733-8627(05)70130-9. PMID 10798893.
- ↑ 20.0 20.1 20.2 Evans RW (1992). "The postconcussion syndrome and the sequelae of mild head injury". Neurologic Clinics. 10 (4): 815–47. doi:10.1016/S0733-8619(18)30182-8. PMID 1435659.
- ↑ Cobb S, Battin B (2004). "Second-impact syndrome". The Journal of School Nursing. 20 (5): 262–7. doi:10.1177/10598405040200050401. PMID 15469376. S2CID 38321305.
{{cite journal}}: CS1 maint: uses authors parameter (link)[permanent dead link]
- ↑ 22.0 22.1 Olver J (2005). "Traumatic brain injury – the need for support and follow up". Australian Family Physician. 34 (4): 269–71. PMID 15861750.
- ↑ 23.0 23.1 "Concussion". online medical library. Merck manuals. 2003. Archived from the original on May 12, 2008. Retrieved May 11, 2008.
- ↑ 24.0 24.1 24.2 24.3 24.4 24.5 24.6 24.7 Iverson GL (2005). "Outcome from mild traumatic brain injury". Current Opinion in Psychiatry. 18 (3): 301–17. doi:10.1097/01.yco.0000165601.29047.ae. PMID 16639155. S2CID 23068406.
- ↑ Iverson GL, Lange RT (2003). "Examination of "postconcussion-like" symptoms in a healthy sample". Applied Neuropsychology. 10 (3): 137–44. doi:10.1207/S15324826AN1003_02. PMID 12890639. S2CID 37015199.
- ↑ King NS (1996). "Emotional, neuropsychological, and organic factors: Their use in the prediction of persisting postconcussion symptoms after moderate and mild head injuries". Journal of Neurology, Neurosurgery, and Psychiatry. 61 (1): 75–81. doi:10.1136/jnnp.61.1.75. PMC 486463. PMID 8676166.
- ↑ "Post-concussion syndrome –Symptoms and causes". Mayo Clinic. Archived from the original on 2017-02-02. Retrieved 2022-04-16.
- ↑ Jorge RE (2005). "Neuropsychiatric consequences of traumatic brain injury: A review of recent findings". Current Opinion in Psychiatry. 18 (3): 289–99. doi:10.1097/01.yco.0000165600.90928.92. PMID 16639154. S2CID 19572299.
- ↑ 29.00 29.01 29.02 29.03 29.04 29.05 29.06 29.07 29.08 29.09 29.10 29.11 Yeates KO, Taylor HG (2005). "Neurobehavioural outcomes of mild head injury in children and adolescents". Pediatric Rehabilitation. 8 (1): 5–16. doi:10.1080/13638490400011199. PMID 15799131. S2CID 23340592.
- ↑ 30.0 30.1 30.2 Jacobson RR (August 1995). "The post-concussional syndrome: physiogenesis, psychogenesis and malingering. An integrative model". Journal of Psychosomatic Research. 39 (6): 675–93. doi:10.1016/0022-3999(95)00006-5. PMID 8568727.
- ↑ Patterson ZR, Holahan MR (2012). "Understanding the neuroinflammatory response following concussion to develop treatment strategies". Front Cell Neurosci. 6: 58. doi:10.3389/fncel.2012.00058. PMC 3520152. PMID 23248582.
- ↑ 32.0 32.1 Bryant RA (2008). "Disentangling mild traumatic brain injury and stress reactions". New England Journal of Medicine. 358 (5): 525–27. doi:10.1056/NEJMe078235. PMID 18234757.
- ↑ 33.0 33.1 33.2 33.3 Lee LK (2007). "Controversies in the sequelae of pediatric mild traumatic brain injury". Pediatric Emergency Care. 23 (8): 580–83. doi:10.1097/PEC.0b013e31813444ea. PMID 17726422. S2CID 33766395.(Subscription required.)[dubious ]
- ↑ 34.0 34.1 34.2 Boake C, McCauley SR, Levin HS, Pedroza C, Contant CF, Song JX, et al. (2005). "Diagnostic criteria for postconcussional syndrome after mild to moderate traumatic brain injury". Journal of Neuropsychiatry and Clinical Neurosciences. 17 (3): 350–56. doi:10.1176/appi.neuropsych.17.3.350. PMID 16179657. Archived from the original on 2006-10-06.
- ↑ ICD-10 Archived 2014-11-02 at the Wayback Machine, International Statistical Classification of Diseases and Related Health Problems 10th Revision (ICD-10) Version for 2010, F07.2 Postconcussional syndrome, World Health Organization.
- ↑ Sivák S, Kurca E, Jancovic D, Petriscák S, Kucera P (2005). "[Contemporary view on mild brain injuries in adult population]" (PDF). Cas. Lek. Cesk. (in slovenčina). 144 (7): 445–50, discussion 451–54. PMID 16161536. Archived from the original (PDF) on 2008-02-27.
- ↑ 37.0 37.1 Mittenberg W, Canyock EM, Condit D, Patton C (2001). "Treatment of post-concussion syndrome following mild head injury". Journal of Clinical and Experimental Neuropsychology. 23 (6): 829–36. doi:10.1076/jcen.23.6.829.1022. PMID 11910547. S2CID 10333031.
- ↑ 38.0 38.1 38.2 Goodyear B, Umetsu D (2002). "Selected issues in forensic neuropsychology". In Van Dorsten B (ed.). Forensic Psychology: From Classroom to Courtroom. New York: Kluwer Academic/Plenum. pp. 289–90. ISBN 0-306-47270-8. Archived from the original on 2022-05-15. Retrieved 2022-04-16.
- ↑ 39.0 39.1 39.2 39.3 39.4 Legome E. 2006. Postconcussive syndrome. Archived 2008-12-01 at the Wayback Machine eMedicine.com. Accessed January 1, 2007.
- ↑ Bazarian JJ, Atabaki S (August 2001). "Predicting postconcussion syndrome after minor traumatic brain injury". Academic Emergency Medicine. 8 (8): 788–95. doi:10.1111/j.1553-2712.2001.tb00208.x. PMID 11483453.
- ↑ Hulshoff Pol HE, Hijman R, Baaré WF, van Eekelen S, van Ree JM (August 2000). "Odor discrimination and task duration in young and older adults". Chemical Senses. 25 (4): 461–64. doi:10.1093/chemse/25.4.461. PMID 10944510. Archived from the original on 2006-09-27. Retrieved 2022-04-16.
- ↑ 42.0 42.1 42.2 Iverson GL, Zasler ND, Lange RT (2006). "Post-concussive disorder". In Zasler ND, Katz DI, Zafonte RD (eds.). Brain Injury Medicine: Principles and Practice. Demos Medical Publishing. pp. 374–85. ISBN 1-888799-93-5. Archived from the original on 2022-05-15. Retrieved 2008-06-05.
- ↑ Rees PM (2003). "Contemporary issues in mild traumatic brain injury". Archives of Physical Medicine and Rehabilitation. 84 (12): 1885–94. doi:10.1016/j.apmr.2003.03.001. PMID 14669199.
- ↑ Schapiro S, Mandel S, Sataloff RT (1993). Minor Head Trauma: Assessment, Management, and Rehabilitation. Berlin: Springer-Verlag. p. 152. ISBN 0-387-97943-3.
- ↑ 45.0 45.1 McCrory, Paul; Meeuwisse, Willem; Dvořák, Jiří; Aubry, Mark; Bailes, Julian; Broglio, Steven; Cantu, Robert C.; Cassidy, David; Echemendia, Ruben J.; Castellani, Rudy J.; Davis, Gavin A. (2017). "Consensus statement on concussion in sport-the 5th international conference on concussion in sport held in Berlin, October 2016". British Journal of Sports Medicine. 51 (11): 838–47. doi:10.1136/bjsports-2017-097699. ISSN 1473-0480. PMID 28446457.
- ↑ 46.0 46.1 Schnadower D, Vazquez H, Lee J, Dayan P, Roskind CG (2007). "Controversies in the evaluation and management of minor blunt head trauma in children". Current Opinion in Pediatrics. 19 (3): 258–64. doi:10.1097/MOP.0b013e3281084e85. PMID 17505183. S2CID 20231463.
- ↑ 47.0 47.1 47.2 47.3 47.4 47.5 47.6 McAllister TW, Arciniegas D (2002). "Evaluation and treatment of postconcussive symptoms". NeuroRehabilitation. 17 (4): 265–83. doi:10.3233/NRE-2002-17402. PMID 12547976.
- ↑ 48.0 48.1 Ropper AH, Gorson KC (2007). "Clinical practice. Concussion". New England Journal of Medicine. 356 (2): 166–72. doi:10.1056/NEJMcp064645. PMID 17215534.
- ↑ 49.0 49.1 Gualtieri CT (1999). "The pharmacologic treatment of mild brain injury". In Varney NR, Roberts RJ (eds.). The Evaluation and Treatment of Mild Traumatic Brain Injury. Hillsdale, N.J.: Lawrence Erlbaum Associates. pp. 411–12. ISBN 0-8058-2394-8.
{{cite book}}: CS1 maint: url-status (link)
- ↑ 50.0 50.1 Alexander MP (1995). "Mild traumatic brain injury: Pathophysiology, natural history, and clinical management". Neurology. 45 (7): 1253–60. doi:10.1212/WNL.45.7.1253. PMID 7617178. S2CID 29479022.
- ↑ https://journal.parker.edu/index.php/jcc/article/download/70/26 Archived 2021-06-18 at the Wayback Machine[bare URL PDF]
- ↑ Duff J (2004). "The Usefulness of Quantitative EEG(QEEG) and Neurotherapy in the Assessment and Treatment of Post-concussion Syndrome". Clinical EEG and Neuroscience. 35 (4): 198–209. doi:10.1177/155005940403500410. PMID 15493535. S2CID 14749417.
- ↑ McCrea 2008, pp. 163–64
- ↑ 54.0 54.1 Komaroff A, Harvard University Harvard Business School (1999). The Harvard Medical School Family Health Guide. New York: Simon & Schuster. p. 359. ISBN 0-684-84703-5.
- ↑ 55.0 55.1 Signoretti, S; Lazzarino, G; Tavazzi, B; Vagnozzi, R (October 2011). "The pathophysiology of concussion". PM&R. 3 (10 Suppl 2): S359–68. doi:10.1016/j.pmrj.2011.07.018. PMID 22035678. S2CID 6161692.
- ↑ Wetjen, NM; Pichelmann, MA; Atkinson, JL (October 2010). "Second impact syndrome: concussion and second injury brain complications". Journal of the American College of Surgeons. 211 (4): 553–7. doi:10.1016/j.jamcollsurg.2010.05.020. PMID 20822744.
although the syndrome might be uncommon
- ↑ Saulle M, Greenwald BD (2012). "Chronic traumatic encephalopathy: a review". Rehabil Res Pract. 2012: 816069. doi:10.1155/2012/816069. PMC 3337491. PMID 22567320.
- ↑ Necajauskaite O, Endziniene M, Jureniene K (2005). "The prevalence, course and clinical features of post-concussion syndrome in children". Medicina (Kaunas). 41 (6): 457–64. PMID 15998982. Archived from the original on 2012-05-13. Retrieved 2022-04-16.
- ↑ 59.0 59.1 Lovell MR, Fazio V; Fazio (February 2008). "Concussion management in the child and adolescent athlete". Current Sports Medicine Reports. 7 (1): 12–15. doi:10.1097/01.CSMR.0000308671.45558.e2. PMID 18296938. S2CID 33758315.
- ↑ Eman Abdulle, Amaal; van der Naalt, Joukje (2020-01-02). "The role of mood, post-traumatic stress, post-concussive symptoms and coping on outcome after MTBI in elderly patients". International Review of Psychiatry. 32 (1): 3–11. doi:10.1080/09540261.2019.1664421. ISSN 0954-0261. PMID 31592690. Archived from the original on 2022-05-15. Retrieved 2022-04-16.
- ↑ "Traumatic Brain Injury: Hope Through Research". nih.gov. NINDS. Publication date February 2002. NIH Publication No. 02-2478. Prepared by: Office of Communications and Public Liaison, National Institute of Neurological Disorders and Stroke, National Institutes of Health. Archived from the original on 2016-12-18. Retrieved 2022-04-16.
- ↑ Yang, Jingzhen; Peek-Asa, Corinne; Covassin, Tracey; Torner, James C. (2015-01-02). "Post-Concussion Symptoms of Depression and Anxiety in Division I Collegiate Athletes". Developmental Neuropsychology. 40 (1): 18–23. doi:10.1080/87565641.2014.973499. ISSN 8756-5641. PMID 25649775. S2CID 4926724. Archived from the original on 2022-01-21. Retrieved 2022-04-16.
- ↑ Yuen, Kit-Man; Tsai, Yi-Hsin; Lin, Wei-Chi; Yang, Chi-Cheng; Huang, Sheng-Jean (2016-09-02). "Retrospectively evaluated preinjury personality traits influence postconcussion symptoms". Applied Neuropsychology: Adult. 23 (5): 322–332. doi:10.1080/23279095.2015.1057638. ISSN 2327-9095. PMID 26786604. S2CID 36551787. Archived from the original on 2022-03-11. Retrieved 2022-04-16.
- ↑ 64.0 64.1 64.2 Benton AL, Levin HS, Eisenberg HM (1989). "Historical notes on the postconcussion syndrome". Mild Head Injury. Oxford [Oxfordshire]: Oxford University Press. pp. 3–5. ISBN 0-19-505301-X.
- ↑ 65.0 65.1 Evans RW (2004). "Post-traumatic headaches". Neurological Clinics. 22 (1): 237–49. doi:10.1016/S0733-8619(03)00097-5. PMID 15062537.
- ↑ 66.0 66.1 66.2 Jones E, Fear NT, Wessely S (November 2007). "Shell shock and mild traumatic brain injury: A historical review". The American Journal of Psychiatry. 164 (11): 1641–45. doi:10.1176/appi.ajp.2007.07071180. PMID 17974926.
- ↑ 67.0 67.1 McCrea, MA (2008). Mild Traumatic Brain Injury and Postconcussion Syndrome: The New Evidence Base for Diagnosis and Treatment. Oxford [Oxfordshire]: Oxford University Press. p. 157. ISBN 978-0-19-532829-5. Archived from the original on 2022-05-15. Retrieved 2022-04-16.
- ↑ Couch JR, Lipton RB, Stewart WF, Scher AI (September 2007). "Head or neck injury increases the risk of chronic daily headache: a population-based study". Neurology. 69 (11): 1169–77. doi:10.1212/01.wnl.0000276985.07981.0a. PMID 17846416. S2CID 26059855.
- ↑ Lew HL, Lin PH, Fuh JL, Wang SJ, Clark DJ, Walker WC (July 2006). "Characteristics and treatment of headache after traumatic brain injury: a focused review". Am J Phys Med Rehabil. 85 (7): 619–27. doi:10.1097/01.phm.0000223235.09931.c0. PMID 16788394. S2CID 31848348.
- ↑ Kasch H, Bach FW, Jensen TS (June 2001). "Handicap after acute whiplash injury: a 1-year prospective study of risk factors". Neurology. 56 (12): 1637–43. doi:10.1212/WNL.56.12.1637. PMID 11425927. S2CID 12734035.
- ↑ Hickling EJ, Blanchard EB, Silverman DJ, Schwarz SP (March 1992). "Motor vehicle accidents, headaches and post-traumatic stress disorder: assessment findings in a consecutive series". Headache. 32 (3): 147–51. doi:10.1111/j.1526-4610.1992.hed3203147.x. PMID 1563947. S2CID 29507787.
- ↑ Jorge R, Robinson RG; Robinson (November 2003). "Mood disorders following traumatic brain injury". Int Rev Psychiatry. 15 (4): 317–27. doi:10.1080/09540260310001606700. PMID 15276953. S2CID 21390231.
- ↑ Abreu, B.C.; Zgaljardic, D.; Borod, J.C.; Seale, G.; Temple, R.O.; Ostir, G.V.; Ottenbacher, K.J. (2009). "Emotional Regulation, Processing, and Recovery After Acquired Brain Injury". In Matuska, K.; Christiansen, C.H.; Polatajko, H.; Davis, J.A. (eds.). Life Balance: Multidisciplinary Theories and Research. Thorofare NJ: SLACK/AOTA Press. pp. 223–40. ISBN 978-1556429064.
- ↑ Jorge RE, Robinson RG, Moser D, Tateno A, Crespo-Facorro B, Arndt S (January 2004). "Major depression following traumatic brain injury". Arch. Gen. Psychiatry. 61 (1): 42–50. doi:10.1001/archpsyc.61.1.42. PMID 14706943.
- ↑ Smith DH (2006). "Postconcussional symptoms not a syndrome". Psychosomatics. 47 (3): 271–72. doi:10.1176/appi.psy.47.3.271. PMID 16684949. Archived from the original on 2008-10-10.
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text:
From the time he joined the priesthood three decades ago, he seemed destined to become a star. As a confidant to two bishops and then as the erudite and clubbable pastor of two churches, Msgr. Kevin Wallin was a towering figure in the Roman Catholic Church in southwestern Connecticut.
Parishioners felt buoyed by his homilies. They hungrily signed up for his far-flung spiritual pilgrimages, flocked to church fund-raisers to catch his melodious voice interpreting show tunes. He attended opera with a man who would become a cardinal and he himself appeared bound for a bishop's miter.
But then about two years ago troubling questions began to be whispered. He acted odd. He was thinner. He walked stooped over. He was absent. Was he sick? Or dying? And then the spicy talk about suspicious men trooping in and out of the rectory.
Finally, last month's revelation. The priest was locked up, charged with dealing crystal methamphetamine.
At a time when priests from California to Delaware have been accused of loathsome deeds, the allegations against Monsignor Wallin, the former pastor of the Cathedral of St. Augustine in Bridgeport, are of a notably different dimension: that he was a drug dealer and addict who was buying an adult novelty shop to launder ill-gotten proceeds, a priest who was cross-dressing and having sex with men.
The enigmatic double lives of Monsignor Wallin burst into public view last month after federal prosecutors announced they had arrested him on charges of possessing and conspiring to sell drugs that could send him to prison for life. Now 61, he languishes in jail, having pleaded not guilty to behavior that many who know him find both twisted and ungraspable.
The Diocese of Bridgeport had forced Monsignor Wallin from his position at St. Augustine in June 2011, after it was alerted to his dissonant behavior. His parishioners were told only of ambiguous personal and health issues. When he balked at accepting help, the diocese quietly stripped him of his priestly functions, but it said it was unaware of any drug dealing.
"What he did in the end was shocking and spiraled out of our control," said Brian Wallace, a spokesman for the diocese. "When we learned about it we took action immediately and forcefully, and regrettably, given how good a priest he was."
The lurid case is only the latest scandal for the Bridgeport Diocese, already tainted by a string of clerical sexual abuse cases. Last year, the Rev. Michael R. Moynihan, the former pastor of St. Michael the Archangel Church in Greenwich, was sent to prison for obstructing justice after being accused of spending church money on himself. In 2007, the Rev. Michael Jude Fay, from St. John Roman Catholic Church in Darien, was convicted of stealing $1.3 million; he died in prison.
Many particulars remain unclear about Monsignor Wallin's tangled life, and his lawyer did not return calls. This depiction is constructed from interviews with members of the clergy and laity who knew him, as well as from court documents.
Monsignor Wallin's fall seems precipitous. But colleagues said that his faith had been weakening for years under the imperatives of running a financially crippled church, and that he had long been sexually active with men. His drug use, they suspect, may have been more recent, and the final tinder that exploded his life.
A dazzling start
The priesthood was his second choice. He began in education.
He was born in Cornwall-on-Hudson, N.Y., and when his parents divorced, he, his mother and two sisters lived with his grandparents on Long Island. He graduated from the State University of New York at Potsdam, then earned a master's from Bowling Green.
For seven years, starting in 1974, he held administrative jobs at SUNY College at Purchase, overseeing student activities and school facilities.
Deciding to become a priest, he enrolled in 1981 in a seminary associated with the Catholic University of America and was ordained in 1984. He told friends: "Being a priest is not what I do. It's who I am."
Starting as a parochial vicar, he presented dazzling oratorical gifts, charisma and indefatigable drive. In 1987, Bishop Walter Curtis, who led the Diocese of Bridgeport, appointed him as his secretary, a prestigious position akin to a combined presidential chief of staff and press secretary.
A year later, the Rev. Edward M. Egan became bishop of Bridgeport and Father Wallin stayed on as his secretary. The Rev. Leo McIlrath, the ecumenical chaplain at the Lutheran Home of Southbury, and others said the two were close and went to Broadway shows, opera and dinners together.
Monsignor Wallin framed the playbills from the many shows he saw. His parish e-mail address became broadwayguy73.
He remained secretary to Bishop Egan until becoming pastor of the Church of St. Peter in Danbury in 1996. Bishop Egan, who went on to become the archbishop of New York and a cardinal, declined to speak about Monsignor Wallin.
In April 2002, Bishop William E. Lori, who had succeeded Bishop Egan as bishop of Bridgeport, appointed Monsignor Wallin to his final post as pastor of St. Augustine, the diocese's mother church. Such was his allure, Mr. McIlrath said, that some Danbury parishioners began attending Mass at St. Augustine. Many imagined him becoming a bishop.
"He was an encyclopedia of church history," said Peter George, 79, a parishioner in Bridgeport. "He was a talented speaker, good in his homilies."
He was involved with many local charities and on the board of Sacred Heart University. He was an important pipeline to wealthy parishioners whose donations were crucial, especially as chaplain to the Order of Malta, an international Roman Catholic charity.
"His lifestyle was go-go-go-go, doing 50 things at once," said a businessman who knew him. "He loved to mix with the big shots."
But there was evidence he was wrestling with his faith. A church worker who has known him for decades described a session with other priests years ago during which they spoke of things like the mercy of God, and Monsignor Wallin said, "You don't really believe that, do you?"
"He had become disillusioned with the bureaucracy of the church," this worker said. "You're always doing the ceremony. You're always dealing with the paperwork. You're not shepherding souls."
This worker and others said the priest had long had sex with men.
'Kevin wouldn't do that'
It began with worries about his mind.
The Rev. Gregg Mecca, 53, a close friend and the pastor at St. Peter, accompanied Monsignor Wallin and some friends to a Broadway musical in early 2011 and found him "very off-kilter." He had shed weight and was fidgety. "I said, 'Kevin, have you seen a doctor? You need to see a doctor,' " Father Mecca recalled.
Several people later asked Father Mecca if he thought Monsignor Wallin was using drugs, "Nah, no way," he replied. "Kevin wouldn't do that."
One close friend mentioned that he sometimes spoke incessantly, and she would have to tune him out. During one round of chattiness, she fell asleep. Monsignor Wallin had lamented to friends the stress of managing his parish. From the time he arrived, the diocese said, St. Augustine, like many inner-city churches, was losing money, and the losses were deepening. The diocese was pumping tens of thousands of dollars a year into it.
A good friend of the priest said he looked like "a refugee from a concentration camp." One day she came to the church to help with paperwork and found that the electricity was shut off for nonpayment.
By April 2011, the diocese began hearing from church workers about his degeneration. "He seemed distracted, more ready to take offense," Mr. Wallace said. "He had nervous facial twitches. His posture wasn't right."
Several people thought he might have Parkinson's disease, or was on the brink of a nervous breakdown.
He would miss appointments. He was three hours late to preside at a wedding.
About the same time, one church worker told diocesan officials that parades of men were visiting Monsignor Wallin at the rectory at all hours. The diocese looked into it, and, as Mr. Wallace said, "We heard enough to believe that he was engaged in sexual activity in the rectory."
Other church workers said he was also involved in cross-dressing, as were some of his visitors.
That June 3, Bishop Lori confronted Monsignor Wallin, who did not entirely refute the revelations. Bishop Lori told him he had to resign. On June 12, the parish was advised he was leaving for health and personal reasons.
After his departure, church officials found a bag stowed in the rectory containing adult pornographic videos, sexual toys and leather masks, according to church workers.
Alarmed at the possibility of child pornography or child abuse, the diocese hired an outside lawyer. The diocese said Monsignor Wallin was questioned and denied interest in children. An expert searched his computer, but found nothing related to children.
The diocese decided it had a priest who had committed a sin but not a crime. Bishop Lori granted him a sabbatical. The diocese hoped that with help, he could fix himself and resume at a new parish. It continued paying him a monthly stipend of about $1,400.
The diocese told him to get a medical evaluation. Months passed. "He was dragging his feet," Mr. Wallace said. "We were, 'Father, when are you going to go?' "
Finally, Bishop Lori ordered him to go. The diocese would not specify where he went, but someone familiar with the case said that he underwent an extensive examination at Johns Hopkins Hospital in Baltimore.
It found that he needed residential treatment to deal with psychological and emotional issues, including excessive narcissism and a penchant for sex. He was also suspected of using drugs.
But he resisted seeking care. On Oct. 7, Bishop Lori suspended his faculties, meaning he was not allowed to act publicly as a priest, a decision the diocese kept private.
On Oct. 31, 2011, Monsignor Wallin agreed to check into St. Luke Institute, a psychiatric hospital in Silver Spring, Md., that treats Catholic clergymen and others. While there, according to some who know him, it was determined that he had been using amphetamines. He left the hospital against staff wishes on Nov. 4.
The next month, Bishop Lori told him that if he did not accept further treatment he could be defrocked.
Again he dithered. A new year arrived. By now, according to authorities, he had changed professions. He had become a drug dealer.
Phones are tapped
He was living in a snug apartment in a matter-of-fact two-story building in Waterbury, in a humble neighborhood of shoebox-shaped apartments. He was also renting the unit across the hall from him, where authorities said a confederate lived.
This was his new demarcated principality, where law enforcement officials said he sold crystal meth. At least once, they said, he hid drugs in a magazine and made the exchange in a parking lot. An informant told agents that the priest was also an addict.
New York drug enforcement agents got on to him from a New York drug distributor who said he met the priest at a party in early 2012 and began buying from him. The man became an informer.
New York agents tipped off Connecticut agents, who enlisted help from the State Police. An undercover officer, according to authorities, made six drug purchases from Monsignor Wallin. Eventually, his phones were tapped.
Authorities said he received his supply from a California couple, Chad McCluskey, 43, who was in the electronics business, and Kristen Laschober, 47, a wardrobe stylist. Both of them filed for bankruptcy last year. They have also been charged in the case and are to be arraigned in Federal District Court in Hartford on Thursday.
Neighbors said men streamed into Monsignor Wallin's apartment, many of them arriving in cars like BMWs and Corvettes. Sounds of sex could be heard.
He stored cases of good wine in the basement, as well as glass pipes and bottles of butane. He was seen doing his laundry, which included lace panties and other articles of women's clothing.
Father Mecca visited him a few times. "Sometimes he was fine and others he was a wreck," he said. "His phone rang a lot, and he texted a lot, but I didn't know what was going on."
One aggrieved neighbor kept a prayer box. Each night, this person dropped a prayer in it that said, "Please God, take the devil out of this house."
Pressured by the diocese, Monsignor Wallin on March 24 entered St. John Vianney Center, a behavioral health treatment center for the clergy and religious in Downingtown, Pa., for a three-month program. He left the hospital after 28 days. The diocese concluded he was delusional about the scale of his issues.
"When he bolted the second time, we knew we had big problems," Mr. Wallace said.
In early May 2012, Bishop Lori issued a decree that suspended Monsignor Wallin from priestly duties, which was circulated among dioceses but not made public.
That month Bishop Lori was installed as archbishop of Baltimore. He declined to be interviewed beyond a statement saying he was praying for Monsignor Wallin. After May, the Bridgeport Diocese said that Monsignor Wallin no longer took its calls. He continued to receive his stipend. But he now fully embraced a darker world.
'I'm whole again'
He was smugly confident about this reconfigured life. When Father Mecca saw Monsignor Wallin soon after he left St. John Vianney, his friend told him that he did not need medical help. "He looked great," Father Mecca said. "I remember him saying, 'You know what, I'm whole again.' "
He decided to give a party on May 16. A tent was put up in the backyard. Scores of people were invited, including prominent public officials and businessmen.
In an e-mailed invitation to what he called his "fandango," he spoke of how "these last 11 months have been perhaps the most unique of my life."
"Despite the challenges and stresses, they have been extremely productive and allowed me to regain my positive perspective and joy in life," the invitation read.
Jim and Barbara Lynch, two admiring parishioners from Danbury, winced when they arrived at his tiny apartment. "I was taken aback," Mr. Lynch said. "He was very thin and looked exhausted."
People trickled in, maybe two or three dozen in all. No luminaries. "It was mostly people we didn't know, guys he'd met along the way," Mrs. Lynch said.
Two months later, Father Mecca accompanied Monsignor Wallin to Cape Cod for four days to, as he put it, "celebrate his recovery." A friend lent them his house.
"We just sat on the deck by the ocean and read and relaxed," Father Mecca said. "It seemed the demons were behind him."
But other things were percolating. Officials said Mr. Wallin was buying an adult toy store in North Haven called Land of Oz and Dorothy's Place. Authorities suspect that he wanted to use it to launder drug money.
Presumably to make the purchase, he incorporated a business called Rahab and Endor. Rahab was a woman mentioned in the Book of Joshua usually described as a prostitute. Endor may refer to the Witch of Endor, a sorceress identified in the Bible.
Monsignor Wallin planned to leave for London on Jan. 3 for 12 days. A longtime friend, who said she knew nothing of his drug life, asked him to go with her and another woman on an educational tour about espionage. She invited him to a dinner party in late December. He seemed vibrant. She asked him if he wanted to resume being a working priest. He told her yes.
On the day his plane left, the law was at his door. His traveling companions arrived in London and for several days tried to discover what had happened to him. His close friend got a call with the answer. She was numb.
Diocese officials said they were unaware of the investigation and did not realize he was in jail for several days, until a deacon who is a police officer heard from another officer.
Soon the word was out.
"You looked at him like he was God, practically," said Charlie Hall, a Danbury parishioner who lives in a shelter. "But now you realize, he's just human, like all the rest of us."
"It's very hard to accept because he was my personal confessor, too," Mr. Lynch said. "We pray for him every day."
On Jan. 22, dressed in a baggy orange jumpsuit, a subdued Monsignor Wallin pleaded not guilty at his arraignment in a Hartford federal court. Prosecutors tabulated that he had grossed more than $300,000 from drug sales.
His Waterbury apartment stands vacant. A picture of Jesus beckons in the window.
Elizabeth Maker and Vivian Yee contributed reporting. Alain Delaquérière contributed research.
This article, "A Dazzling Priest's Lurid Fall, to Drug Case Suspect," first appeared in The New York Times.

subset: commoncrawl


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St-Germain Paris in the Spring Event
Sugar + Shake went to Addiction nightclub at The Modern Honolulu hotel for a celebration of St-Germain liqueur and Grey Goose introducing the new St-Germain carafes. Sugar's note on the photos in this gallery: "Since St-Germain has this whole retro Paris thing going on, I decided to process all the photos with a vintage-y look. Admittedly, this technique also covers a multitude of sins, such as the soft focus and high noise I ended up with, and the weird lighting because this was a nightclub with oddball colored lights going off all the time." © Sugar + ShakeRead More


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I've loved the Co-op since I first started commenting and posting there in February 2010. The original gang of four were discussing Wounded By School and I was so intrigued by the level of candor and openness, and the honest, respectful, grounded-in-practice kind of talk that was going on there that I decided to get in and stay around, if they'd have me. (I remember Paula White saying, "Aren't we all wounded by school?" Hell yes I thought to myself!)
What did I love about the Co-op? For one, this was (and is) a place where strong-minded, well-read, well-tweeted and social networked teachers, principals, superintendents, parents and many others concerned about education could talk about what frustrates them about their work, and what they should do about it. How powerless they sometimes feel in the face of seemingly insurmountable odds against real educational transformation. About the ways school seems to actively reproduce the inequality and passivity they are committed to working against, and their intimate struggles and successes with teaching. And most importantly, what they are actually doing and making happen. Since then, the Co-op has organized two national reform efforts, grown from a group of four to 51 regular posters, watched several organizations grow (Monika Hardy's lab, IDEA), yet retains its distinctive respectful, thoughtful, it's-okay-to-be-vulnerable-here feel. (Peter Skillen brought up the problem of teacher ego getting in the way of release of control to students only recently.) Chad Sansing reminds us almost every day in every comment what it's like to be a successful practitioner and still be trying to weigh and balance who you are, and to be open about what we don't know.
I writing to say that I think we have to widen the circle, and strengthen our circle beyond what largely appears to be White, Progressive-minded, transformation-interested educators at relatively well-resourced schools, who live part of their learning lives online. We need to bring in folks who represent other points of view, who are interested in similar projects, and who will help us know better what we don't know, and what we aren't talking about.
As Beverly Daniel Tatum says in Can We Talk About Race, as schools dramatically resegregate in our country by class, socioeconomics and race–as they precipitously and agonizingly do, more and more with every passing year–our face-to-face social networks in school shrink and "the likelihood of at least one interracial friendship or a multiracial social network," diminishes. As Monika reminded me this summer, through Ethan Zuckerman's TEDTalk, the economic and racial divide on Twitter, and our online lives, is real. If we allow it here, we all lose.
Who is NOT a part of the conversation here? Who should be here? Whom, from your network, can you invite in here, to comment, to guest post, to perhaps become a part of the circle, if he or she wishes?
- I am inviting the awesome and fiery Jose Vilson to guest post here, if he'll have us.
- I am inviting my colleague Bernard Gassaway, former principal of Beach Channel High School in Queens, NY to post here, if he has time.
- I am inviting my friend Winston Benjamin, youth activist and educator who works only with students who "have been rejected from school," to join the conversation.
- I am inviting my friend Aldo, who is a student at a small charter high school in Chelsea, MA who immigrated from Mexico City when he was fourteen, and was recently accepted to college, to post here.
How can we widen the circle?
Who are you bringing in?


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B-Mobile announced the b-micro TalkingSIM Platinum Service and the b-microSIM for the iPhone 4.
B-Mobile seems to be moving towards offering two types of data plans: 1) a symmetric 300 kbps plan with restrictions on streaming for around ¥3000 per month, and 2) a platinum plan offering higher speed, as well as streaming, for about ¥6000 per month. The platinum plan also supports tethering a PC via USB or bluetooth, but at only 300 kbps.
However, there is an issue to overcome: tethering.
The b-micro TalkingSIM platinum allows higher speed access, though not necessarily unrestricted access to Docomo's 7.2 Mbps network, only for certain apps, which are referred to as the "iPhone 4 exclusive network." (The iPad is not listed as supported.) As far as I can tell, any other traffic would be restricted to 300 kbps. This will allow the use of data-hungry apps like youtube and skype, while negating the risk of excessive packet use via a tethered PC.
Of course I would like to see the U300 data-only SIM and the TalkingSIM offered in two flavors, regular and platinum, with no restrictions on platforms (as long as it is certified for use in Japan), and in two sizes, regular and micro, but I don't see how B-Mobile can accomplish this without getting burned in packet costs paid to Docomo.
Here are the whitelisted apps.
- Mobile Safari
- App Store
- Apple Mail app
- iTunes (Podcast)
- radiko
- YouTube (Mobile version)
- Ustream live Broardcast
- Google Maps app
- evernote
- Dropbox
- Skype
- ¥3150 one-time new contract registration fee
- ¥6,260 base fee (includes unlimited data)
- ¥1,050 voice fee (25 free included minutes)
- Additional minutes @ ¥21/half minute (same typical rate of the big three carriers)
- No information on SMS price
Pricing for the b-microSIM is the same as their full-sized data SIM, and so is the speed, 300 kbps. I also assume the TOS will be similar, which, if they are, means no credit card and proof of residency required. iPad is not supported Well, perhaps it is and the website simply does not reflect it. After all, we've had a number of reports of chopped down U300's working in iPads.
- 1 year for 29,800 yen
- 6 months for 14,900 yen
- 1 month for 2980 yen.


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To my regular readers, I must interrupt my 18 Things blog tour to bring you this special message:
Neumarian Uprising
We need your help! Thanks to our spy, Ciara Knight, we are able to communicate with you today via blogs, Facebook, Twitter and other social media.
The Neumarian uprising has begun. We are fighting for freedom and equality for all, but we need your help. Ciara informed us that you might want to know more about the uprising and why we ask you to risk your lives for our cause. To answer these questions I've agreed to let Ciara tell my sister's, Raeth's, story about her captivity. It will be free for you on a site called Amazon until March 1, 2013.
Our spies have told us this will help spread the word and find more recruits for our rebellion against the tyrannical queen. You can help by simply downloading a free copy of Weighted, a prequel to the Neumarian Chronicles. If you are intrigued and wish to follow our uprising, Escapement, book I of The Neumarian Chronicles, will be available for only $2.99 until March 1, 2013.
Escapement is told by Princess Semara. Don't hold the fact Semara is a princess against her like I did, there is more to her than you can possibly imagine.
Here is a brief explanation of her telling of our uprising:
Ten years after the great war of 2185 the queen's reign is threatened by uprisings and fear. In celebration of my sixteenth birthday it is my duty as princess to sacrifice a slave to be initiated into the ruling council, solidifying my mother's empire. When my own erratic powers surface I'm captured and tried for treason. Slaves hate me, my mother wants me executed, and my only chance of survival rests in the hands of a young man, Ryder Arteres, whose sister I sentenced to death.
What people are saying about Escapement:
"A heady mix of action adventure and steampunk — leavened with a dash of romance — ESCAPEMENT offers up its fair share of thrills, horrors and heart-pounding moments. A strong start to a captivating new series."
— Jana Oliver, author of The Demon Trapper's Daughter
"A riveting tale of justice, mercy, honor and love. Take a deep breath and hold on, because you'll be turning the pages of Escapement quickly. Three unlikely comrades, Princess Semara, Ryder, and his sister Raeth, embark on a journey that will alter their lives forever. The beautiful love story nestled into these action-packed scenes will make you sigh and remember why you love to love. After reading the prequel Weighted, I knew this story would be amazing, and it was. Ciara Knight truly has a gift for creating awesome worlds and characters you won't forget."
–Lindi Peterson–Award winning author of Summer's Song.
"Betrayal, secrets, and a rebellion send readers on a grand adventure, caught in the plight to discover Semara's gifts and purpose."
–Alex J Cavanaugh, author of Amazon best sellers CassaStar and CassaFire
"The most unmissable series ever! I couldn't stop reading, the action and romance too breathtaking to break the spell!"
–ARC review by Sudah on Goodreads
"A courageous heart-stopping journey by young people to save their kind."
–Hildie McQueen, bestselling author of Where the Four Winds Collide
If you'd like to see a peak into our world, please view this short clip on You Tube.
If you are now ready to join our fight, please add Escapement to your TBR shelf on Goodreads here. Shout out on all your social media sites, and tell everyone you know to stand up and fight.
Be Bold.
Be Brave.
Be Free.
In the name of the rebellion,
Ryder Arteres
Escapement can be found at Amazon.
Wonderful cover, right?! I know we all have a rebellion to join, but you'll want to keep querying those agents and editors in the meantime if you're a writer like me! So stop by Pk Hrezo's blog today for the tidbits of wisdom I learned from my local RWA writer's conference this past weekend! Just two more stops of the 18 Things blog tour this week before it's all finished *phew, wipes forehead*
But tell me before you hop over, are you gonna join the Neumarian Uprising?!


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Our intern, Ariel Holcomb, is visiting us from Seattle this summer. It's always a treat —this one in particular!—to hear about her favorite findings as she explores New York City:
Last night, in order to escape the sweltering New York City heat, I decided to check out the newest addition to the High Line, a New York City park that was once an elevated rail road track. It serves as both a concrete oasis and a place to see a spectacular view of the sun setting over the Hudson River. The High Line has attracted bars, restaurants, and galleries to the surrounding neighborhood which was once the city's meat packing district, transforming it into a chic urban hangout where you can sample some of the latest trends in food, one of them being artisanal frozen treats! It's where you can find Coolhaus, a mobile food truck that allows you to pick your favorite flavor of ice cream and pair it with your preferred kind of cookie to create the ultimate ice cream sandwich. Customized ice cream sandwiches – sounds like a dream come true!
Combinations like Ginger Snap Cookies and Lemon Meyer Ice Cream or Oatmeal Raisin Cookieswith Pumpkin Pie Ice Cream are imaginative takes on a classic treat. In addition to New York City, there are Coolhaus trucks roaming Los Angeles, and Austin. However don't worry if you live elsewhere, you can create your own ice cream sandwich right at home. Use any cookie recipe from Good Housekeeping's test kitchen and pair it with your favorite ice cream flavor and brand.
More From Good Housekeeping
Trying to keep it low-cal? Try Breyers Smooth and Dreamy low-fat ice cream, the winner in the Good Housekeeping Research Institute (GHRI)'s low-calorie ice cream taste test, as your sandwich filling. Some of the combos I'm going to try are Double Chocolate Cherry Drops with vanilla ice cream, Peanut Butter Thumb Prints with strawberry ice cream and Chocolate Chippers and espresso ice cream! If you really want to customize your ice cream sandwiches, use homemade ice cream. Need an ice cream maker? See Sharon Franke, GHRI's Kitchen Appliance Director's post on The Best Ice Cream Makers.


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Arenachicks Summer Tour was HUGE Success
Posted by admin | Posted in News | Posted on 18-08-2012
Thank you ICP,NWA All-Stars, CWF Mid-atlantic, Dukes of Hazzard Festival crew and most of all…all of the girls who participated. It's an amazing opportunity to travel and work with your friends. Amber O'neal and the Arenachicks documented the summer tour and it will be released in a few months. Here is a preview trailer from footage we filmed during this amazing experience.


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Multnomah Boulevard Stormwater Retrofits
Multnomah Boulevard is major transportation corridor and stormwater runoff from the street carries pollutants to Tryon and Verrmont creeks. In 2011, Environmental Services constructed stormwater planters and swales that capture stormwater and allow it to soak into the ground. Vegetation and soil in the planters filter pollutants.


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Quick post to describe how to apply a gradient mask to a display object in AS3 (& AS2).
#1 Put your gradient mask on the stage – lets call it gmask
#2 Put the object to be masked on the stage.
#3 Set both the mask and the 'object to be masked' to cacheAsBitmap
#4 Apply the mask to the object
In #AS3
gmask.cacheAsBitmap = true
obj_to_be_masked.cacheAsBitmap = true
obj_to_be_masked.mask =gmask
In #AS2
gmask.cacheAsBitmap = true
obj_to_be_masked.cacheAsBitmap = true
It really is as simple as this.
Note to designers: Gradient masks can't obviously be done directly from the IDE (see below), but these three lines can be placed on the timeline if so desired.
To put a gradient mask on dynamic text you will need to place the text within a container (movieclip/sprite) and mask that.
The object to be masked can also contain animation, text or video though this will require a bit more processor as the bitmap will need to redraw on each frame. Often this is well worth it as the effect can be great.
There is a way of achieving this same effect with no code at all and here it is:
#1 Put your gradient mask on the stage – lets call it gmask
#2 Put the object to be masked on the stage.
#3 Put both of these items into a movieclip/sprite (the container) making sure the mask is on a layer above the object
#4 Give the mask a blend mode of 'Alpha'
#5 Give the 'container' a blend mode of 'Layer'
And there you have it. Gradient masking achieved with blendModes and absolutely no code.
Benchmarking the two gradient mask methods:
I used each method to mask an embedded video – then placed an instance on the display list and ran at varying frame rates.
Initially there was negligible difference between the code and blend mask methods. I ramped up the FPS to 120 and put four instances of the video on screen. With this set up the code method (cacheAsBitmap) was up to 4% faster than the blendMode Mask method.
Conclusion: The code method is faster but very marginally. If you are desperate for a bit of extra juice go with code.


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I never know what to make of reports stating the "accuracy" of some test or detection algorithm. Take this example, from a New York Times article by Steve Lohr titled How Privacy Vanishes Online:
In a class project at the Massachusetts Institute of Technology that received some attention last year, Carter Jernigan and Behram Mistree analyzed more than 4,000 Facebook profiles of students, including links to friends who said they were gay. The pair was able to predict, with 78 percent accuracy, whether a profile belonged to a gay male.
I have no idea what "78 percent accuracy" means in this context. The most obvious answer would seem to be that of all 4,000 profiles analyzed, 78% were correctly classified as gay versus not gay. But if that's the case, I have an algorithm that beats the pants off of theirs. Are you ready for it?
Say that everybody is not gay.
Figure that around 5 to 10 percent of the population is gay. If these 4,000 students are representative of that, then saying not gay every time will yield an "accuracy" of 90-95%.
But wait — maybe by "accuracy" they mean what percentage of gay people are correctly identified as such. In that case, I have an algorithm that will be 100% accurate by that standard. Ready?
Say that everybody is gay.
You can see how silly this gets. To understand how good the test is, you need two numbers: sensitivity and specificity. My algorithms each turn out to be 100% on one and 0% on the other. Which means that they're both crap. (A good test needs to be high on both.) I am hoping that the MIT class's algorithm was a little better, and the useful numbers just didn't get translated. But this news report tells us nothing that we need to know to evaluate it.


text: Because of so many songs colleges out there, it may get overwhelming when choosing the right one for you. So before you distribute programs, surface initially using a simple selection of colleges that you simply feel may help you reach your possible as being a music performer. When narrowing across the collection, be sure to… Continue reading Finding the Right Music School


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London, England (CNN) -- Although his name is synonymous with horror, Christopher Lee says he doesn't have much desire to see pictures that fall under that genre these days.
The 87-year-old, who helped Britain's legendary Hammer studios breathe new life into the horror genre in the 1950s, says he rarely watches horror films.
"I find it quite nauseating what they do," Lee told CNN. "The blood is all over the screen like an avalanche -- the mutilation -- dreadful things, and I just don't enjoy that."
The veteran actor, who played Count Dracula and Frankenstein in a series of Hammer movies from the 1950s until the 1970s, says it's "obscene" how much is displayed in horror films today.
"What you don't see is far more frightening than what you do see," said Lee, who considers Roman Polanski's 1968 supernatural thriller "Rosemary's Baby" the scariest film he's ever seen.
That may explain his attraction to upcoming psychological chiller "The Resident," his first Hammer film in more than 30 years.
Starring Hilary Swank and Jeffrey Dean Morgan, the movie is about a young doctor whose landlord develops a creepy obsession with her.
Lee was a perfect fit for the film, which takes on a nightmarish quality in a nod to the noir style of Alfred Hitchcock, director Antti Jokinen says.
"He has that presence that a movie like this needs because a single look can be the scary atmosphere that you need," Jokinen told CNN.
"The Resident," due out in the spring, is the first theatrical feature under the banner of the re-launched Hammer Films. It is being revived by new investors who bought the company two years ago.
Lee says his reunion with Hammer is ironic in a way. He didn't leave the studio on the best of terms -- "I'm not going to go into it, but take it from me, they ruined it," he says of his last Hammer film, bizarre 1976 cult classic "To the Devil a Daughter."
Some remarkable films did come out of that era: He describes black-and-white "Scream of Fear" (1961) as "brilliant," and fondly recalls working with the close-knit Hammer team, which was like a family.
"Occasionally they'd change the cameraman or something but otherwise the whole crew was the same all the time, and I knew all of them extremely well," he said.
But the white-haired actor doesn't wax nostalgic. "Not every Hammer film was perfect," he said.
In 1966's "Prince of Darkness," he ended up playing the character of Dracula silent because the lines "were not good and I couldn't do anything with them."
Lee played a central role in the rise of Hammer, starring in 1958's "Dracula," which helped both him and the studio gain international recognition.
The film was instrumental in launching a golden era for the production house, whose films, with their gothic qualities and use of vibrant colors, helped reinvigorate the horror genre.
But the movies began to seem outdated as movies like "The Exorcist" and "The Omen" came on the scene, and Hammer produced its last film in 1976.
Lee -- or to be precise, Sir Christopher Lee, after Queen Elizabeth II knighted him in June -- has come a long way since his first Dracula film, a six-week job that he says paid £750.
Although he's often associated with Hammer films, Lee is quick to point out that he hasn't really taken many horror roles.
Aside from the Dracula movies, "The Curse of Frankenstein" (1957) and "The Mummy" (1959), "I haven't done lots of horror," the prolific actor told CNN.
Of course, that hasn't kept him from achieving cult status among horror fans.
Included in his legion of fans is "The Resident" co-star Morgan, who says he "hit the ceiling with excitement" when he found out Lee was joining the cast.
Morgan told CNN: "He's got this kind of dignity to him that's just great.
"I work with so many actors that don't have respect for what we do, or respect for the history of what we do and not only does he respect it, but he is a part of the history of this craft."
Over the decades Lee has starred in hundreds of movies. He has a predilection for playing baddies, including Bond villain Scaramanga in "The Man with the Golden Gun" (1974).
"I haven't spent my entire career playing the guy in the bad hat, although I have to say that the bad guy is frequently much more interesting than the good guy," Lee said.
His more recent film credits include the menacing Saruman in the "Lord of the Rings" trilogy and fallen Jedi knight Count Dooku in the Star Wars prequels.
But he considers 1973's "The Wicker Man" "the best picture I've ever done." The role was written for him and remains his favorite.
"They didn't have to look for me to play the part; they wrote the part for me," which doesn't happen very often, he said.
Lee has kept a busy work schedule. In addition to "The Resident," he stars alongside Colin Farrell in the soon-to-be-released "Triage," is involved in a film from the director of "The Wicker Man" and lends his voice to animated film "Monstermania!"
Lee, who doesn't show any signs of slowing down, despite approaching the age of 90, is pragmatic about his extraordinary career.
"Well," he said. "What else would I do?"


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Spencer-East Brookfield superintendent granted personal leave
Staff Writer
Telegram & Gazette
The Spencer-East Brookfield School Committee last night agreed to grant School Superintendent Reza Namin a personal leave.
Mr. Namin said the leave is effective immediately and he is unsure how long he will be away from his job.
He said he needs to attend to personal matters, including moving to a house he owns in Northboro. He has been staying at a hotel and traveling between here and Maine, where his wife lives in their home, since accepting the job in Spencer more than a year ago.
School Committee members named Debora Zablocki, principal at Lake Street School, as acting superintendent during his absence. One member, Kurt Nordquist, voted against that move.
— Kim Ring


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A Powerpop Trifecta at Bowery Electric
Wednesday night at Bowery Electric, Don Piper and his group opened the evening with a richly melodic, often hypnotic set. Piper's primary gig these days is producing great albums – the Oxygen Ponies' lushly layered, darkly psychedelic classic Harmony Handgrenade is one of his credits – but he's also a bandleader. This time out he alternated between slowly swirling, atmospheric, artsy rock and a vintage Memphis soul sound, backed by a large, spirited crew including keyboards, a two-piece horn section (with Ray Sapirstein from Lenny Molotov's band on cornet), bass and the Silos' Konrad Meissner on drums (doing double duty tonight, as would many of the other musicians). Midway through the set Briana Winter took over centerstage and held the crowd silent with her wary, austerely intense, Linda Thompson-esque voice on a couple of midtempo ballads. They closed with a long, 1960s style soul number, Piper and Winter joining in a big crescendo as the band slowly circled behind them.
Edward Rogers followed, backed by much of the same band including Piper, Meissner, Claudia Chopek on violin and Ward White playing bass. A British expat, Rogers' wry, lyrical songs draw on pretty much every good British pop style through the mid-70s. The most modern-sounding song, a pounding, insistent number, evoked the Psychedelic Furs, White throwing in some Ventures-style tremolo-picking on his bass at a point where nobody seemed to be looking. Whatever You've Been Told, from Rogers' latest album Sparkle Lane, held an impassioned, uneasy ambience that brought to mind early David Bowie. A pensive, midtempo backbeat tune with a refrain about the "seventh string on your guitar, the one you never use" reminded of the Move (like Roy Wood, Rogers hails from Birmingham), as did a bracingly dark new one, Porcelain, highlighted by some striking, acidic violin from Chopek. And a pair of Beatles homages wouldn't have been out of place on the Rutles albums – or George's later work with Jeff Lynne. But the best songs were the most original ones. The most stunning moment of the night came on the understatedly bitter Passing the Sunshine, a Moody Blues-inflected requiem for an edgy downtown New York destroyed by greedy developers, gentrifiers and the permanent-tourist class: "This'll be the last time you steal with your lies," Rogers insisted, over and over again. In its gentle, resolute way, it was as powerful as punk. They wound up the show with a surprisingly bouncy psychedelic pop tune and then the new album's droll, swaying title track.
Seeing headliner Maura Kennedy onstage with a bright red Les Paul slung from her shoulder was a surprise, as it was to see her guitar genius husband Pete Kennedy in the back with the drums, leaving most of the solos to his wife. But as fans of their acoustic project the Kennedys know, she's an excellent player – and also one of the most unselfconsciously soulful voices in rock, or folk, if you want to call them that. This was her powerpop set, many of the songs adding a subtly Beatlesque or Americana edge to fast new wave guitar pop. The best songs were the darker ones, including the bitterly pulsing 1960s style psych/pop hit Just the Rain. Sun Burns Gold swayed hauntingly and plaintively, leaving just a crack for the light to get in; another minor-key number, Chains was absolutely gorgeous in a jangly Dancing Barefoot garage-pop vein, and she used that as a springboard for one of several sharply staccato, chordally charged solos. "I wrap myself in melancholy comfort of the waiting game," she sang on a brooding ballad that evoked Richard and Linda Thompson. But there were just as many upbeat moments. White, who was doing double duty despite being under the weather, took an unexpected and welcome bass solo on a funkily hypnotic number toward the end of the set; they wound it up with the first song she'd written, she said, the country-pop ballad Summer Coulda Lasted Forever. The rest of the musicians joined them for an amazingly tight, completely deadpan cover of A Day in the Life, Maura leading her little orchestra with split-second precision all the way through the two long, interminable crescendos, a wry vocal from her husband on Paul's verse, and then up and up and up some more and then finally out. It was an apt way to end a night of similarly expert craftsmanship.


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It was Val's birthday and Name Day today (St Katherine of Alexandria), and we had a pretty busy day. First we went to the Hours and Readers Service at Mamelodi, and then went to the annual prizegiving at St Athanasius School in Tembisa, with the monks from St Thomas's Orthodox Church in Sunninghill. Here is Val with Fr Evsevije (Eusebius).
At the prizegiving just about all the children got certificates for something, and several of them presented plays or sang songs.
For a fuller report see my Khanya blog.
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