The characterization of cognitive deterioration processes is still clinical, with imaging tests (MRI or PET) being a support tool in some occasions. The first option would be the correct one because it allows us to measure in a standardized way each of the cognitive domains, which will allow us to frame the patient's deficits in a specific syndrome and to monitor the deterioration with repeated scans over time.

The characterization of cognitive deterioration processes is still clinical, with imaging tests (MRI or PET) being a support tool in some occasions. The first option would be [HIDDEN] because it allows us to measure in a standardized way each of the cognitive domains, which will allow us to frame the patient's deficits in a specific syndrome and to monitor the deterioration with repeated scans over time.

A 72-year-old patient presents with progressive memory loss and word finding difficulty of one year's duration. What is the most useful examination to characterize the type of cognitive deficit he presents with?

Progressive amnestic cognitive impairment in a middle-aged patient with developmental language disorder: a case report.

Developmental disorder and dementia in older adults have been considered unrelated clinical entities because their timing of diagnosis differs greatly; however, recent studies have suggested an association between them. This case describes a middle-aged patient with language disorder exhibiting progressive amnestic cognitive impairment. A 44-year-old Japanese man with long-term language dysfunction presented for his first-ever medical evaluation at age 36 years. Although his conversational ability had been impaired since childhood, he was able to graduate from secondary school and gain unskilled employment. At age 36 years, however, his workplace environment became more stressful, which led to behavioral problems that necessitated medical consultation. He consulted two psychiatrists in vain. At age 44 years, the third attending psychiatrist examined him in detail. The major component of his language disorder was amnestic cognitive impairment in the language domain as shown by logical memory subtests of the Wechsler Memory Scale-Revised. Magnetic resonance imaging showed normal findings for his age and no small vessel disease. Global cerebral hypoperfusion versus cerebellar blood flow was shown on (<sup123</supI) iodoamphetamine single-photon emission computed tomography, and amyloid-β deposition was negative on positron emission tomography with <sup11</supC-Pittsburgh compound B. Pathologic tau accumulation was negative on <sup18</supF-THK5351 positron emission tomography imaging. Laboratory tests show no infections, no vitamin deficiencies, and no other diseases that may cause dementia. Clinical features, results of neurocognitive tests and neuroimaging studies showed no well-known neurodegenerative diseases. Collectively, he was diagnosed with language disorder based on the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition criteria. Over a 2-year follow-up period, amnestic cognitive impairment in visual and language domains progressed in parallel with global cerebral hypoperfusion. This case suggests a possible link between language disorder as defined by Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition criteria and progressive amnestic cognitive impairment in middle age, which may ultimately lead to dementia, derived from a neurodegenerative disease.

Pseudodementia

A significant overlap in cognitive and neuropsychological dysfunction in Dementia and pseudodementia patients increases the difficulty in diagnosis. Differences in the severity of impairment and quality of patients' responses can be observed, and a test of antisaccadic movements may be used to differentiate the two, as pseudodementia patients have poorer performance on this test. Individuals with pseudodementia present considerable cognitive deficits, including disorders in learning, memory and psychomotor performance. Substantial evidences from brain imaging such as CT scanning and positron emission tomography (PET) have also revealed abnormalities in brain structure and function. A comparison between dementia and pseudodementia is shown below.

[A clinicopathological study of young-onset dementia: report of 2 autopsied cases].

We retrospectively examined the clinical features and the neuroradiological findings on autopsy of 2 cases of young-onset dementia. The patient in case 1 was a 43-year-old woman who was unable to determine the time on the clock and who made frivolous remarks. Neuropsychological test batteries demonstrated memory impairment and frontal lobe dysfunction. T2-weighted magnetic resonance imaging (MRI) of the head revealed abnormal high-intensity signals around the lateral ventricles and thinning of the corpus callosum. Single photon emission computed tomography (SPECT) revealed patchy reduction in the accumulation of tracers in both the frontal lobes. Her neurological condition gradually deteriorated, and she died 13 years after the onset of the disease. She was clinically diagnosed with atypical Alzheimer's disease on the basis of visual cognitive impairment and memory impairment observed in the initial phase. However, the neuropathological diagnosis was adult-onset leukodystrophy with axonal spheroids. The patient in case 2 was a 43-year-old man who had gradually started behaving selfishly and had become ill-tempered and apathetic. He was admitted to a hospital. He was anosognosic and showed frontal lobe dysfunction. T2-weighted MRI scan of the brain showed abnormal high-intensity signals around the lateral ventricles; atrophy of the frontal and temporal lobes, hippocampus, and brainstem; and thinning of the corpus callosum. SPECT revealed patchy reduction in the accumulation of tracers in both the frontal lobes and the cerebellum. His neurological condition gradually deteriorated, and he died after being clinically ill for 7 years. The patient was clinically diagnosed with frontotemporal dementia on the basis of the clinical features and MRI findings. However, the neuropathological diagnosis was chronic meningoencephalitis. The frequency of neurological metabolic and inflammatory diseases is significantly high although it is not as high as that of degenerative diseases in young-onset dementia. Since such diseases may respond to therapy, they should be considered in the differential diagnosis of young-onset dementia, especially in patients presenting with atypical clinical features. Neuroradiological examination may contribute to the differential diagnosis of atypical dementia at young age.

[Dementia with frontal lobe atrophy: clinical study from 18 patients with cognitive impairment and frontal lobe involvement detected by structural and functional neuroimaging].

To characterize clinically patients with cognitive impairment and frontal lobe degeneration at neuroimaging. Patients diagnosed of dementia or mild neurocognitive impairment by DSM IV criteria and neuropsychological tests with frontal lobe atrophy and hipoperfusion detected by computed tomography and single photon emission computed tomography. 18 patients, 5:1 on behalf of women; mean age at onset, 74 years; hereditary for dementia, 38%; mean duration of illness at first testing, 2 years; the most common initial symptoms, memory loss. At initial examination, psychotic or behavioral impairment was found in 61% and parkinsonism in 38%, the commonest cognitive troubles at this moment was the executive function, language and anterograde memory dysfunctions at the same rate. Frontal lobe atrophy and hypoperfusion was found in 100%, temporal in 88% and parietal in 38%. Electroencephalogram was pathological in 33%. The course of the disease was progressive but with fluctuation in 27%. Frontotemporal dementia clinical criteria in 13 patients, 4 of them clinical criteria of dementia with Lewy bodies too, and clinical criteria of Alzheimer s disease in 5.

Brain metabolism as measured with positron emission tomography: serial assessment in a patient with familial Alzheimer's disease.

This paper presents, for the first time, repeated assessments of cerebral metabolism and neuropsychological competence in early Alzheimer's disease. Regional cerebral metabolic rates for glucose were measured with positron emission tomography and 18F-fluoro-2-deoxy-D-glucose on three occasions at 8-month intervals, in a 57-year-old man with Alzheimer's disease of 2 1/2 years' duration and with a family history of neuropathologically confirmed Alzheimer's disease. Data were compared with mean cerebral metabolic rates from 12 healthy men. No differences in regional cerebral metabolic rates for glucose were found on the initial patient scan, whereas metabolism on the second and third scans was reduced significantly in the parietal lobes and bilaterally in some parietal lobe regions. Memory loss was demonstrable at the first scan, but then and at later scans, other aspects of cognitive performance remained within normal limits (Wechsler Adult Intelligence Scale, Boston Naming Test, Two-dimensional Block Construction). The results show that memory loss can precede a measurable reduction of cerebral metabolism in early Alzheimer's disease, but that later reductions in parietal lobe metabolism may not be accompanied by additional measurable neuropsychological deficits.

Report of a Case of Creutzfeldt-Jakob Disease With an Unusual Clinical Presentation.

We describe the clinical features, neuropsychological tests, laboratory, electroencephalography (EEG), magnetic resonance imaging (MRI) and positron emission tomography (PET) findings of a 59-year-old woman who presented to our Centre for cognitive impairment since few months, with language disturbances, particularly anomia, dyscalculia, and memory loss. The clinical and neuropsychological features were non-specific and overlapping with those of other rapidly progressing neurodegenerative disorders. However, brain MRI played a pivotal role in the diagnosis, showing cortical diffusion restriction, particularly in the parietal lobes and posterior cingulum, with sparing of the perirolandic cortex, typical of Creutzfeldt-Jakob disease (CJD). Brain MRI abnormalities were visible since the first evaluation and remained stable at 2 and 6 weeks follow up. Basal ganglia and thalami were never involved. PET showed left lateralized reduced glucose metabolism, with partial overlap with MRI signal abnormalities. Despite MRI were strongly indicative of CJD, clinical, laboratory and EEG findings did not fulfill the diagnostic criteria for CJD which applied at the time of clinical assessment. Indeed, neither myoclonus, visual or cerebellar signs or akinetic mutism were present. Also, the characteristic periodic sharp wave complexes were absent at baseline EEG, and the CSF assay for 14-3-3 was negative. We, therefore, performed a real-time quaking-induced conversion (RT-QuIC) assay on a frozen sample of corticospinal fluid (CSF), which showed a positive result. RT-QuIC is a prion protein conversion assay that has shown high diagnostic sensitivity and specificity for the diagnosis of CJD. RT-QuIC has been recently incorporated in the National CJD Research and Surveillance Unit and Center for Disease Control and Prevention (CDC) diagnostic criteria for CJD. The fatal evolution of the disease brought the patient to death 13 months after symptoms onset. Pathology proved the diagnosis of sporadic CJD, subtype MM/MV 2C.

Difficulty with learning of exercise instructions associated with 'working memory' dysfunction and frontal glucose hypometabolism in a patient with very mild subcortical vascular dementia with knee osteoarthritis.

We present a patient with no dementia, depression or apathy, who had difficulty in learning self-exercise instructions. The patient was an 80-year-old right-handed woman who was admitted to a rehabilitation unit to receive postoperative rehabilitation after a femoral neck fracture. She was instructed quadriceps isometric exercises to perform 10 repetitions and to hold each stretch for 10 s. She performed the exercise correctly with motivation, but she had difficulty in learning the number of repetitions and the duration of each stretch. She had no history of cerebrovascular accident and the neurological examination was normal. Neuropsychological testing, MRI and (18)F-fluoro- D-glucose-positron emission tomography (FDG-PET) were performed to examine the neural mechanisms associated with this difficulty in learning instructions. Neuropsychological tests revealed dysfunction of working memory while other cognitive domains were relatively preserved. Her neuropsychological tests scores were (1) Mini-Mental State Examination: 24 (mild cognitive impairment), (2) Geriatric Depression Scale-15: 2 (no depression), (3) Apathy Scale: 2 (no apathy), (4) digit span forward: 5 (normal), (5) digit span backward: 2 (impaired), (6) visuospatial span forward: 4 (normal), (7) visuospatial span backward: 2 (impaired), (8) frontal assessment battery: 11 (normal), (9) Weigl test: 0 (impaired), (10) trail making test A: 52 s (normal), (11) train making test B: failed (impaired). T2-weighted and fluid-attenuated inversion recovery MRI showed high signal-intensity lesions in the cerebral deep white matter. FDG-PET revealed hypometabolic areas in the bilateral frontal lobes, particularly in the bilateral dorsolateral frontal area, anterior cingulate cortex and orbitofrontal cortex. One of the possible neural mechanisms underlying the learning difficulties in this patient may have been partial blockage of the cingulofrontal network by deep white matter lesions.

[Slowly progressive memory impairment without generalized dementia--a clinical and radiological study].

We report a patient with a ten-year history of slowly progressive recent memory decline without additional cognitive impairment in presenility. A right-handed Japanese barber first experienced forgetfulness at the age of 59. Neurological examination at age 64 revealed no abnormality except for severe impairment in memorizing. Brain CT-scans were normal. In spite of gradually deteriorating memory, he was capable of organizing his work until the age of 67 years. At age 69, he showed intense recent memory defect and disorientation in time, but immediate memory span and remote memory beyond the retrograde gap were better preserved. Intelligence quotient (IQ) on the Wechsler adult intelligence scale-R remained 85 (verbal IQ, 88: performance IQ, 83). Neurological examination was negative. He showed no signs of aphasia, agnosia, or apraxia. Minimal organic personality changes were noticed. Brain CT-scans and MRI revealed mild atrophy of the temporal lobes and hippocampal formation on both sides. I123-IMP single photon emission computed tomography (SPECT) disclosed a decrease of cerebral blood flow in both the inferior temporal and superior frontal regions. SPECT after acetazolamide administration showed augmented accumulation in areas with decreased accumulation at baseline. Despite progressive memory impairment, the absence of aphasia, agnosia, or apraxia differentiates our case from more common Alzheimer's disease. A degenerative disorder of focal cerebral atrophy or "simple senile dementia" of presenile onset was suspected of causing the underlying pathophysiological changes.

Semantic memory

Present and future research Semantic memory has had a comeback in interest in the past 15 years, due in part to the development of functional neuroimaging methods such as positron emission tomography (PET) and functional magnetic resonance imaging (fMRI), which have been used to address some of the central questions about our understanding of semantic memory. Positron emission tomography (PET) and functional magnetic resonance (fMRI) allow cognitive neuroscientists to explore different hypotheses concerning the neural network organization of semantic memory. By using these neuroimaging techniques researchers can observe the brain activity of participants while they perform cognitive tasks. These tasks can include, but are not limited to, naming objects, deciding if two stimuli belong in the same object category, or matching pictures to their written or spoken names.

[A case of primary progressive multiple sclerosis with onset of memory impairment].

We report a 52-year-old woman with primary progressive multiple sclerosis (PPMS) presenting with chronic progressive memory impairment. From a couple of years prior to admission, she had developed impairment of her short-term memory. For example, she forgot her nephew's name, and spoke the same phrases again and again. She also sometimes forgot to turn off her gas stove and forgot things she bought in shops. Moreover, her mental activity gradually decreased and she became apathetic. However, she did not note her memory impairment, and had no hallucinations. She was admitted to our hospital on 20 May, 2003 because donepezil had been ineffective for treating her memory impairment. Neurologically, she showed bilateral horizontal gaze nystagmus, mild limb ataxia on the left and mildly ataxic gait. Neuropsychological examinations showed mildly impaired cognitive function, e.g., MMSE 25/30, WAIS-R full IQ 69 and especially in verbal short memory, which may represent temporal lobe dysfunction. Moreover, Benton's visual memory test revealed marked visual short-term memory impairment, while impaired performance on a Kana picking up test suggested mild to moderate attention impairment, which could have represented frontal lobe dysfunction. Brain MRI showed multiple T2-high plaque lesions close to the bilateral lateral ventricles, and bilateral optic nerve lesions enhanced by gadolinium. Also, spinal cord MRI showed a gadolinium enhanced lesion at Th5 on the left. Cerebral spinal fluid (CSF) examination showed normal cell count and protein level, and undetectable oligoclonal bands (OCB), but an elevated IgG index (1.1, normal < 0.85). Visual evoked potentials (VEPs) showed prolonged P100 latency bilaterally, indicating subclinical optic nerve lesions. She was thus diagnosed as having PPMS according to McDonald's diagnostic criteria for MS. 99mTc Single photon emission computed tomography (SPECT) showed a decreased cerebral blood flow (CBF) in the bilateral frontal and temporal lobes, which was consistent with her clinical features. PPMS patients generally present with chronic progressive spastic paraparesis and/or cerebellar ataxia. Cognitive impairments observed in PPMS are generally thought to be due to white matter lesions, i.e., subcortical dementia. However, some recent reports have shown MS patients with short-term memory impairment (antegrade amnesia) similar to cortical dementias such as Alzheimer's disease (AD). In such MS cases, visual short-term memory impairment seems characteristic of their cognitive impairment compared to AD cases. As well, the present case showed visual memory impairment as evaluated by Benton's memory test. Parietal and frontal lobes are reported to be important for verbal and visual working memory, respectively. Thus, in the present case, decreased CBF in the frontal and temporal lobes, which could have been due to a disconnection between cortices and subcortices caused by the white matter lesions, is consistent with the type of her cognitive dysfunction, i.e., notable visual memory impairment. PPMS may thus be an important disease as a differential diagnosis for chronic progressive dementia. Further neuropsychological and functional imaging studies will be necessary to achieve a better understanding of the mechanisms of cognitive impairment in PPMS.

Sleep and memory

Neural imaging measures Neuroimaging can be classified into two categories, both used in varying situations depending on what type of information is needed. Structural imaging deals predominately with the structure of the brain (computed tomography) while functional imaging deals more heavily with metabolic processes in regards to anatomical functioning (positron emission tomography, functional magnetic resonance imaging). In recent years, the relationship between sleep and memory processes had been aided by the development of such neuroimaging techniques. Positron emission tomography (PET) is used in viewing a functional processes of the brain (or other body parts). A Positron-emitting radionuclide is injected into the bloodstream and emits gamma rays which are detected by an imaging scanner. Computer analysis then allows for a 3-dimensional reconstruction of the brain region or body part of interest.

[Presenile dementia with marked recent memory disturbance--in relation to hippocampal dementia].

Two cases of presenile dementia with marked recent memory disturbance were reported. Patient 1 is a 54-year-old woman. She noticed forgetfulness at the age of 51 years. Neurological examination at aged 52 revealed marked recent memory disturbance, but examination by WAIS (Wechsler Adult Intelligence Scale) showed good results (verbal IQ 106, performance IQ 104, total IQ 106). There was neither disorientation in place nor character change. Cranial CT scan and MRI revealed the absence of brain atrophy. About 3 years after the onset of the disease, the degree of dementia is slight and disorientation in place does not appear. Patient 2 is a 67-year-old man. He noticed forgetfulness at the age of 63 years. Neurological examination at aged 66 revealed marked recent memory disturbance, but examination by WAIS-R showed moderate results (verbal IQ 89, performance IQ 87, total IQ 88). There was neither disorientation in place nor character change. Cranial CT scan and MRI revealed slight dilatation of the inferior horns of the lateral ventricle and slight cortical atrophy. About 4 years after the onset of the disease, the degree of dementia was slight and disorientation in place did not appear. We can not rule out the possibility that our cases belong to Alzheimer's disease, but the clinical course of our cases is peculiar. In the relation of responsible lesion in pure amnestic syndrome, hippocampal dementia, and simple senile dementia, our cases are interesting and important.

Cognitive neuropsychology

With improved neuroimaging techniques, it has been possible to correlate patterns of impairment with a knowledge of exactly which parts of the nervous system are damaged, allowing previously undiscovered functional relationships to be explored (the lesion method). Contemporary cognitive neuropsychology uses many of the same techniques and technologies from the wider science of neuropsychology and fields such as cognitive neuroscience. These may include neuroimaging, electrophysiology and neuropsychological tests to measure either brain function or psychological performance. Useful technology in cognitive neuropsychology includes positron-emission tomography (PET) and functional magnetic resonance imaging (fMRI). These techniques make it possible to identify the areas of the brain responsible for performing certain cognitive tasks by measuring blood flow in the brain. PET scans sense the low-level radiation in the brain and produce 3-D images, whereas an fMRI works on a magnetic signal

CDC classification system for HIV infection

Cryptosporidiosis or isosporiasis with diarrhea persisting more than 1 month Cytomegalovirus disease with onset of symptoms at age over 1 month (at a site other than liver, spleen, or lymph nodes) Encephalopathy (at least one of the following progressive findings present for at least 2 months in the absence of a concurrent illness other than HIV infection that could explain the findings): a) failure to attain or loss of developmental milestones or loss of intellectual ability, verified by standard developmental scale or neuropsychological tests; b) impaired brain growth or acquired microcephaly demonstrated by head circumference measurements or brain atrophy demonstrated by computerized tomography or magnetic resonance imaging (serial imaging is required for children under 2 years of age); c) acquired symmetric motor deficit manifested by two or more of the following: paresis, pathologic reflexes, ataxia, or gait disturbance

Hanna Damasio

Hanna Damasio utilizes brain imaging methods, such as computerized tomography and nuclear magnetic resonance, to enhance the diagnoses protocols for diseases that affect the brain. Her current projects include: developing new techniques to investigate brain structure in vivo using magnetic resonance, developing new techniques to evaluate experimental results in positron emission tomography (PET), and investigating the neuroanatomical substrates of language, memory, emotion, and decision-making using the lesion method. Her work has resulted in numerous scientific articles which appeared in leading journals. In 1989, she published "Lesion Analysis in Neuropsychology" (Oxford University Press), a classic textbook for which she received the Prize for Outstanding Book of the Year in Bio and Medical Sciences from the Association of American Publishers. Her continued interest in human neuroanatomy led her to develop the first atlas of the human brain based on computer tomography images:

Detection of early amnestic mild cognitive impairment without significantly objective memory impairment: a case-controlled study.

We encountered eight early amnestic mild cognitive impairment (aMCI) patients (early MCI group) who did not fulfill the diagnostic criteria for aMCI. We compared the scores of neuropsychological examinations as well as the cerebral metabolic rate for glucose consumption (CMRglc) decrease on (18)F-FDG PET examination between the early MCI group and 10 aMCI patients (MCI group) or six normal elderly subjects (normal group), to examine whether the current diagnostic criteria can detect early-stage aMCI. The three groups underwent Mini-Mental State Examination (MMSE), Wechsler Adult Intelligence Scale - Third Edition (WAIS-III), Wechsler Memory Scale Revised (WMS-R), magnetic resonance imaging and 18F-fluorodeoxyglucose positron emission tomography ((18)F-FDG PET) examinations. The early MCI group did not show significant memory impairment of 1.0 SD or other cognitive dysfunctions on neuropsychological examinations, and did not fulfill the diagnostic criteria of aMCI. With one-way anova and Tukey's HSD post-hoc test, the early MCI group showed the highest scores for WAIS-III, whereas the MCI group showed the lowest scores for WMS-R, although there were no significant differences between the early MCI and normal groups. In order to show a discrepancy in scores between WAIS-III and WMS-R, we subtracted the scores of WMS-R from WAIS-III. Consequently, the normal group showed significantly smaller differences in scores than the other groups, although there were no significant differences between the early MCI and MCI groups. (18)F-FDG PET recognized a CMRglc decrease in the posterior cingulate gyrus and/or part of the parietotemporal area in both the MCI and early MCI groups, of which the extent and magnitude were weaker in the early MCI group. The normal group did not show a significant CMRglc. The early MCI group should be included in aMCI not only based on the discrepancy between intelligence and memory scores, but also based on the (18)F-FDG PET findings. The combination of these examinations would make it possible to diagnose early-stage aMCI.

A case of atypical progressive supranuclear palsy.

Progressive supranuclear palsy (PSP) is a neurodegenerative extrapyramidal syndrome. Studies have demonstrated that PSP can present clinically as an atypical dementing syndrome dominated by a progressive apraxia of speech (AOS) and aphasia. We aimed to investigate the clinical presentation of PSP, using a comprehensive multidimensional evaluation, and the disease response to various pharmacological treatments. A 72-year-old right-handed male, with 17 years education, who first presented with aphasia, AOS, depression, apathy, and postural instability at 69 years; a complete neuropsychological evaluation, tapping the different cognitive domains, was performed. Testing revealed a moderate global cognitive deficit (Mini-Mental State Examination test score =20), low memory test scores (story recall, Rey's 15-word Immediate and Delayed Recall), and poor phonemic and semantic fluency. The patient's language was characterized by AOS, with slow speech rate, prolonged intervals between syllables and words, decreased articulatory accuracy, sound distortions, and anomia. Behavioral changes, such as depression, anxiety, apathy, and irritability, were reported. The neurological examination revealed supranuclear vertical gaze palsy, poor face miming, and a mild balance deficit. Magnetic resonance imaging showed only widespread cortical atrophy. Single photon emission computed tomography demonstrated left > right frontotemporal cortical abnormalities. After 6 months, a further neuropsychological assessment showed a progression in cognitive deficits, with additional attention deficits. The patient reported frequent falls, but the neurological deficits remained unchanged. Neuroimaging tests showed the same brain involvement. Our case highlights the heterogeneity of the clinical features in this syndrome, demonstrating that atypical PSP can present as AOS and aphasia, without the classical features or involvement of the subcortical gray and brainstem region, commonly affected in typical PSP.

Epilepsy surgery in the elderly: an unusual case of a 75-year-old man with recurrent status epilepticus.

Epilepsy surgery is increasingly well-supported as an effective treatment for patients with intractable epilepsy. It is most often performed on younger patients and the safety and efficacy of epilepsy surgery in elderly patients are not frequently described. We report a case of a 75-year-old right-handed man who underwent a left fronto-temporal craniotomy for resection of a suprasellar meningioma in 2002. Immediately following hospital discharge, he began to experience complex partial seizures. He continued to have frequent seizures despite treatment with multiple combinations of antiepileptic medications. He presented with status epilepticus every two or three months, and required long periods of hospitalization on each occasion for post-ictal confusion and aphasia. Scalp EEG showed continuous spikes and polyspikes and persistent slowing in the left temporal area, as well as spikes in the left frontal area. EEG telemetry recorded multiple seizures, all with a clear focus in the left temporal area. MRI scan showed an area of encephalomalacia in the left temporal lobe, as well as post-surgical changes in the left frontal area. Neuropsychological testing showed bilateral memory impairment with no significant cognitive decline expected after unilateral temporal lobe resection. A left anteromesial temporal lobectomy was performed with intraoperative electrocorticography. Since surgery, the patient was not seizure-free (Engel class II-b), but had no further episodes of status epilepticus in one year and two months of follow-up. This is one of the oldest patients reported in the literature with epilepsy surgery and supports the possibility of epilepsy surgery in elderly patients for particular cases. In addition, few cases with such a malignant evolution of temporal lobe epilepsy have been described in this age group.

List of medical tests

Neurological electroencephalogram electromyography (EMG) lumbar puncture neuropsychological tests Obstetric / Gynaecological amniocentesis colposcopy mammography hysteroscopy laparoscopy Smear tests such as Pap smears Ocular dilated fundus examination multifocal electroretinography (mfERG) optical coherence tomography (OCT) visual field test Pulmonary polysomnography pulmonary pletysmography thoracentesis Radiology CT scan (B*2****) magnetic resonance imaging (MRI) (B*3****) nuclear medicine (C******) positron-emission tomography (PET) projectional radiography (B*0****) ultrasonography (B*4****) Rheumatologic arthroscopy Urologic cystoscopy urodynamic testing References Tests Tests

A case series of epilepsy-derived memory impairment resembling Alzheimer disease.

We report 4 cases of epilepsy-derived progressive memory disturbances that clinically resembled Alzheimer disease. The patients were 3 women and 1 man, aged 56 to 79 years. The greatest disturbance was in recent memory. The patients' remote memory and orientation were relatively intact. Mental dullness and a decline in daily activities were also observed. No overt seizures were observed in any of the patients. Electroencephalography (EEG) revealed spikes in the left temporal region in 3 patients and in the left central region in the other patient. Single photon emission computed tomography or positron emission tomography revealed focal areas of hypofunction in the frontal, parietal, and parietotemporal regions. Performance of activities and memory improved rapidly in all patients after treatment with carbamazepine; the improvement was maintained after more than a year. It might be speculated that epileptic discharges caused dysfunction in the temporal lobe and the remote cortex through the neocortical and mesiotemporal network. EEG would be useful to rule out the possibility of a reversible condition in patients with cognitive disturbance. Moreover, investigation of this epilepsy-related condition with the combination of EEG and neurofunctional imaging might provide clues to clarify the pathophysiology of Alzheimer disease.

Neurosyphilis presenting with unusual hippocampal abnormalities on magnetic resonance imaging and positron emission tomography scans: a case report.

The incidence of neurosyphilis has declined markedly since the introduction of penicillin therapy. While there are a number of case reports in the literature of neurosyphilis causing focal decreased 18F-fluorodeoxyglucose uptake on positron emission tomography/computed tomography scans, to the best of our knowledge this is the first published report of neurosyphilis presenting with intensely increased 18F-fluorodeoxyglucose uptake in the hippocampus. A 55-year-old Caucasian man presented to our facility with acute collapse against a background of memory difficulties over the previous six months. The results of his initial physical examination were normal. He scored 24 out of 30 on the Montreal Cognitive Assessment test. A magnetic resonance imaging scan of his brain revealed high T2 signal intensity and atrophy within the right frontal area in addition to high T2 signal intensity in the bilateral mesial temporal areas. Blood and cerebrospinal fluid analysis revealed an active syphilis infection. An 18F-fluorodeoxyglucose positron emission tomography brain scan showed intensely increased 18F-fluorodeoxyglucose uptake limited to the head of the right hippocampus. He responded to penicillin treatment with an improvement in his cognition, which was further reflected in a complete resolution of the findings previously seen on magnetic resonance imaging and 18F-fluorodeoxyglucose positron emission tomography scans. Diagnosis of neurosyphilis can be difficult, as many patients are either asymptomatic or present with non-specific symptoms such as memory disturbance or seizures. This report highlights the importance of considering neurosyphilis in the differential diagnosis when mesiotemporal changes are seen on magnetic resonance imaging or 18F-fluorodeoxyglucose positron emission tomography scans.

A follow-up study of the family with the Swedish APP 670/671 Alzheimer's disease mutation.

To study the progression of Alzheimer's disease (AD) at a very early stage and to evaluate clinical markers of presymptomatic AD. Longitudinal study at a university hospital. A Swedish family harboring a double mutation at codons 670/671 of the APP gene on chromosome 21 was followed longitudinally for 3 years. Both mutation carriers and noncarriers participated. Results from clinical investigations, electroencephalography, neuropsychological and neuroradiological examinations including magnetic resonance imaging, single-photon emission computed tomography and positron emission tomography were assessed and compared on two or more occasions. During follow-up, 1 initially asymptomatic mutation carrier who was near the expected age of onset for this family, developed cognitive symptoms, and at the end of the follow-up fulfilled the diagnostic criteria for AD. One mutation carrier with cognitive symptoms at the first examination showed clinical deterioration and was diagnosed with AD. One demented mutation carrier died and was shown to have typical AD neuropathology at autopsy. The two remaining asymptomatic mutation carriers, as well as all the noncarriers were asymptomatic. These mutation carriers who were near the expected age of onset of AD but without clinical signs of the disease, did not show changes in either electrophysiological parameters or volumes of the temporal lobes. However, in these 2 individuals the blood flow in the temporal lobe showed intermediate values between the symptomatic mutation carriers and healthy noncarriers. Two neuropsychological tests showed a deterioration that paralleled clinical symptoms in 1 of the mutation carriers who was close to the expected age of onset and who at the end of the follow-up had clinical signs of AD. In the same subject, brain glucose metabolism was pathologically reduced in the temporal lobes before other clinical symptoms were obvious. In this familial form of AD a reduced temporal lobe glucose metabolism was indicative of AD before the expected clinical onset. Reduced glucose metabolism even preceded the development of subjective or objective cognitive dysfunction and might therefore serve as a clinical marker for AD before the onset of clinical symptoms. Reduced cerebral blood flow in the temporal lobes and cognitive deterioration paralleled the clinical decline in the early stage of the disease. Copyrightz1999S.KargerAG,Basel

Alzheimer disease and nonfluent progressive aphasia.

To describe a patient with pathologically proven Alzheimer disease (AD) who presented with a non-fluent progressive aphasic syndrome. Longitudinal neuropsychological assessment, structural (magnetic resonance imaging) and functional (single photon emission computed tomography) imaging, and postmortem brain examination. Memory and cognitive disorders clinic in a tertiary referral hospital. A 66-year-old man presented with a 5-year history of progressive nonfluent aphasia characterized by marked deficits in phonology and syntax with preservation of everyday abilities. His condition deteriorated rapidly and he died suddenly of a myocardial infarction 12 months later. Neuropsychological testing revealed mild global intellectual impairment with marked impairment of auditory verbal short-term memory, syntactic, and phonological abilities. His naming errors were predominantly phonological paraphasias. Magnetic resonance imaging scans showed left perisylvian atrophy and results of a Tc 99m hexamethyl-propyleneamine-oxime single photon emission computed tomographic scan were normal. Postmortem pathological examination revealed typical AD pathological features with atypical distribution, involving predominantly perisylvian language areas, but sparing the medial temporal lobe. The language deficits in AD, which have received considerable attention, are thought to involve predominantly lexicosemantic processes. When AD presents as a relatively isolated language disturbance, the aphasia is usually of the fluent anomic type. To our knowledge, our patient represents the first fully documented case of progressive nonfluent aphasia with pathologically verified AD.

[A case of atypical presenile dementia].

Kosaka (1993) reviewed 16 cases of slowly progressive presenile cortical dementia thought to be a clinicopathological entity with pathological features characterized by circumscribed lobar atrophy, diffuse neurofibrillary tangles, and calcification of the Fahr type, however, the clilical features of this new entity are not known in the description of detail. We report a patient with atypical presenile dementia which appeared to be consistant with that entity, together with the results of a comprehensive neuropsychological and neuroradiological examination. The patient was a 65-year-old right-handed housewife. At about 58 years of age, she started to lose spontaneity and develop a mild memory disturbance. At age 61 she transiently, experienced hallucinations and delusions. During the subsequent 8 years there was a very slight decline in global intellectual efficiency. In addition, she showed slow but definite progression of language disturbances characterized by anomia and loss of ability to grasp the meaning of words, particularly abstract nouns. She performed poorly on tasks with good sensitivity for detecting frontal lobe dysfunction, such as the Wisconsin Card Sorting Test and the hand sequence test. All other cognitive functions appeared to be relatively well preserved, however moderate dyscalculia was present. There was no socially inappropriate or stereotyped behavior, but the patient lost insight into her disease. The patient's activities of daily living on the ward were self-maintained. An EEG was normal. CT and MRI scans showed circumscribed bilateral fronto-temporal atrophy and bilateral mineralization in the basal ganglia and cerebellar white matter.(ABSTRACT TRUNCATED AT 250 WORDS)

Neuropsychology

Brain scans The use of brain scans to investigate the structure or function of the brain is common, either as simply a way of better assessing brain injury with high resolution pictures, or by examining the relative activations of different brain areas. Such technologies may include fMRI (functional magnetic resonance imaging) and positron emission tomography (PET), which yields data related to functioning, as well as MRI (magnetic resonance imaging) and computed axial tomography (CAT or CT), which yields structural data. Global Brain Project Brain models based on mouse and monkey have been developed based on theoretical neuroscience involving working memory and attention, while mapping brain activity based on time constants validated by measurements of neuronal activity in various layers of the brain. These methods also map to decision states of behavior in simple tasks that involve binary outcomes.

Cognitive function in non-demented individuals complaining of short-term memory disturbances: a study with event-related potentials (P 300) and brain CT scan.

Event-related potentials (ERPs) were elicited in 30, non-consecutive, non-demented individuals, complaining of short-term memory disturbances. Fifteen of them had a moderate diffuse cerebral atrophy on their brain CT and the other 15 had a negative brain CT. ERPs were also elicited in 15 age-matched controls with no reported memory disturbances and negative brain CTs. The statistical analysis showed that the group of individuals with cerebral atrophy had a significantly prolonged P300 (P3) latency and a decreased P3 amplitude compared to controls. It is concluded that among persons complaining of short-term memory disturbances, the individuals who show cerebral atrophy, taken as a group, have a P3 latency prolongation and/or low P3 amplitude a finding which reflects an impaired information processing.

Rehabilitation (neuropsychology)

[Devastating epileptic encephalopathy-pseudoencephalitis: the new type of catastrophe epilepsy in our department].

Analysis of history of our five patients with intractable epilepsy whose illness have begun with prolonged status epilepticus (SE) and high-grade fever of unknown cause. Retrospective study analysis of selected five intractable epileptic patients at a median age of 11.5 (8-14) years. All children had normal development before epilepsy begun. Intractable SE lasted 3-10 (median seven) days by four patients and three months by one patient. The cause of illness was unknown at the beginning and the MRI were normal. Intractable epilepsy followed the SE in all cases without any latent period. Follow-up of the children was 3-15 (median 9.5) years. The seizures came continually with few-day-long breaks, antiepileptic drugs were ineffective. Semiology of seizures, EEG, and functional imaging examinations (PET, SPECT) referred to temporal and frontal lobe damages. Later on, the MR images showed hippocampal sclerosis in one patient and mild generalized brain atrophy in the others. During the years, cognitive deterioration and behavioral problems have been realized. The most severe patient developed tetraparesis, fell in vigil coma and died after five years. The symptoms of our patients fulfilled the criteria of devastating epileptic encephalopathy in school-aged children.

Implicit memory

Neuropsychology has used imaging techniques such as PET (positron emission tomography) and MRI (magnetic resonance imaging) to study brain-injured patients, and has shown that explicit memory relies on the integrity of the medial temporal lobe (rhinal, perirhinal and parahippocampal cortex), the frontal–basal areas and the bilateral functionality of the hippocampus. The amygdala is mainly responsible for the emotional component in the process of information storage (see Gazzaniga, 1999; Mancia, 2000b, 2004, in press), and can modulate both the encoding and the storage of hippocampal-dependent memories (Phelps, 2004). Implicit memory, by contrast, is not conscious and concerns data that can be neither remembered nor verbalized. It presides over the learning of various skills: a) priming, which is the ability of an individual to choose an object to which he has previously been exposed subliminally; b) procedural memory, which concerns cognitive and sensorimotor experiences such as motor

[A 83 year-old woman with dementia, gait disturbance, and convulsion].

We report a 83 year-old woman with dementia. She was apparently well until December of 1993 when she was 81-year-old. At that time, she was operated or her cataract. Her post operative course was uneventful, however, shortly after her operation, she had an onset of memory loss and abnormal behavior. She showed a fluctuating course in her mental disturbance. In 1995, her dementia worsened with nocturnal agitation. She was admitted to our service on June 12, 1995. She was alert and her blood pressure was 140/100 mmHg. She showed recent memory loss and disorientation to time. Motor wise, she was unable to stand unsupported. Her gait with support showed small steps and a wide base. She was bradykinetic and ataxic in her finger-to-nose and heel-to-knee test, however, no rigidity or tremor was noted. Her MRI showed T2-high signal lesions in both medial thalamic areas, in the right occipital lobe, and in the bilateral cerebral white matters as well as in the basal ganglia. She was discharged for out-patient follow up on July 3, 1995. Four days after the discharge, she showed declining responses to stimuli and she developed dyspnea on July 14, 1995. She was admitted again on the same day. Her body temperature was 38.5 degrees C and moist rales were heard in the left lung field. She appeared drowsy and no verbal response was obtained; no apparent motor palsy was noted. Blood count showed leukocytosis (14,300/ml). Blood gas analysis under 61 of oxygen inhalation through a mask was as follows: pH 7.460, PCO2 39.6 mmHg, PO2 67 mmHg, and HCO3-28.5 mEq/l. Two days after admission, she developed a convulsion in her left arm and she became unconscious. Her EEG showed periodically recurring lateralized epileptic discharges on the right fronto-central areas. Her subsequent course was complicated by status epilepticus and respiratory distress. She died on July 26, 1995. She was discussed in a neurological CPC. The chief discussant arrived at a conclusion that she suffered from multi-infarct dementia. Bilateral thalamic infarctions were considered to have played a significant role in her dementia. Post-mortem examination revealed subcortical leukoencephalopathy of Binswanger's type and cerebral infarctions in the thalamic and basal ganglia regions and in the right occipital lobe. In addition, she showed isolated angitis of the central nervous system involving mainly in the small arteries located in the superficial areas of the brain and the spinal cord. This patient was interesting in that despite relatively mild leukoaraiosis in MRI, post-mortem examination revealed profound pathologic changes in the subcortical white matters. In addition, she showed the isolated angitis of the CNS. The cause and the clinical correlates of her angitis were unclear.

Functional neuroimaging

Functional neuroimaging is the use of neuroimaging technology to measure an aspect of brain function, often with a view to understanding the relationship between activity in certain brain areas and specific mental functions. It is primarily used as a research tool in cognitive neuroscience, cognitive psychology, neuropsychology, and social neuroscience. Overview Common methods of functional neuroimaging include Positron emission tomography (PET) Functional magnetic resonance imaging (fMRI) Electroencephalography (EEG) Magnetoencephalography (MEG) Functional near-infrared spectroscopy (fNIRS) Single-photon emission computed tomography (SPECT) Functional ultrasound imaging (fUS)

Isolated amnesia with slow onset and stable course, without ensuing dementia: MRI and PET data and a six-year neuropsychological follow-up.

Patient EDS presented with an amnesic disorder of insidious onset (4 years) that remained stable and restricted to memory functions over a 10-year course. Repeated neuropsychological evaluations over 6 years showed a moderate-to-severe, stable impairment of long-term memory and of memory for public events, and a milder, stable impairment of autobiographic memory and of short-term memory. Language, perception, praxis and 'frontal' functions were fully preserved. MRI showed atrophy of the right hippocampus, of the right mammillary body and of the sylvian fissure (bilaterally, but more marked on the left). On PET scan, metabolic activity in the mesial temporal structures was significantly reduced on the right and was at lower normal levels on the left. The disorder observed in EDS is similar to that recently reported in other patients. Possible etiologies of the selective amnesia observed in EDS are considered and their implications discussed.


He describes S1 root involvement by the inability to tiptoe and the absence of the Achilles reflex, in addition to the distribution of pain down the leg. Of our options, the cause that can produce damage to S1 is L5-S1 disc herniation.

He describes S1 root involvement by the inability to tiptoe and the absence of the Achilles reflex, in addition to the distribution of pain down the leg. Of our options, the cause that can produce damage to S1 is [HIDDEN].

A 53-year-old man with no history of interest who after a bad movement in the gym notices low back pain that after a few hours radiates to the back of the right leg and reaches the lateral edge of the foot. On examination he presents positive Lasègue maneuver at 40o, abolished hamstring reflex and he cannot stand on tiptoe. The most probable etiological diagnosis is:

Spontaneous regression of a large sequestered lumbar disc herniation: a case report and literature review.

Lumbar disc herniation is a common disorder in adults that is accompanied by lower back and radicular pain. A 32-year-old man visited our clinic with 1-week history of persistent lower back pain and weakness in his right big toe. Magnetic resonance imaging (MRI) of his lumbar spine revealed herniated discs at L3/L4, L5/S1 and L4/L5, where a right-sided intraspinal mass lesion deep to the L4 vertebral body was causing compression of the nerve root. The patient underwent conservative treatment and reported no symptoms referrable to his back or leg 4 months later. Follow-up MRI showed no herniation of the nucleus pulposus at the L4/L5 level or lesion deep to the vertebral body of L4, whereas no changes had occurred to the status of the herniated L3/L4 and L5/S1 discs. The present case and a literature review show that a sequestered lumbar disc herniation can regress within a relatively short timeframe without surgery. The authors emphasise the utility of conservative therapy for patients who do not have a definitive surgical indication.

Report of an Isolated L5 Radiculopathy Caused by an L2-3 Disc Herniation and Review of the Literature.

Intervertebral disc herniation is a common cause of radiculopathy. Disc herniations occurring in the lumbar spine typically affect the nerve root exiting under the pedicle of the vertebral body, one level caudal. However, in rare cases, a disc herniation can cause remote isolated radicular symptoms. The authors present the case of a 70-year-old male who presented with an acute, new-onset, left-sided foot drop, low back pain, and a classic L5 monoradiculopathy. Imaging revealed a large, left-sided paracentral extruded L2-3 disc and the absence of any pathology at the L4/5 level. Although the patient's clinical presentation and imaging did not classically correlate, it was felt that the L2-L3 disc was the etiology of the patient's L5 radiculopathy and a left L2-3 microsurgical discectomy was performed. At the six-week follow-up, his foot drop was near normal, sensation was intact with minimal paresthesias, and he remained pain-free. At the one-year follow-up, he experienced full resolution of his foot drop and remained symptom-free. Although rare, disc herniations may cause isolated, remote, painful mononeuropathies not related to the direct level of nerve root compression and should be considered along with other etiologies of peripheral neuropathies.

Lumbar Disc Herniation -- History and Physical

A straight leg raise test is a neurological maneuver performed while examining a patient presenting with lower back pain. It is conducted with the patient lying supine while keeping the symptomatic leg straight by flexing the quadriceps. The examiner slowly elevates the leg progressively at a slow pace. The test is positive when it reproduces the patient's symptoms (pain and paresthesia) at an angle lower than 45 degrees with radiation below the knee (Lasegue sign). It is most helpful in diagnosing L4, L5, and S1 radiculopathies. The patient is asked to dorsiflex the foot while the examiner is raising the leg (Bragaad's sign) to increase the sensitivity of the test.

L5 nerve root exits at the L5-S1 foramina. When compressed by a herniated disc, it causes back pain that radiates into the buttock, lateral thigh, lateral calf, the dorsum of the foot, and the great toe. Sensory loss is present on the web space between the big toe and second toe, the dorsum of the foot, and lateral calf. There is a weakness in hip abduction, knee flexion, foot dorsiflexion, big toe dorsiflexion, foot inversion, and eversion. Patients present with decreased semitendinosus/semimembranosus reflex. Weakness in foot dorsiflexion makes it challenging to walk on the heels. Chronic L5 radiculopathy may cause atrophy of the extensor digitorum brevis and the tibialis anterior of the anterior leg.

Extreme lateral lumbar disc herniation: clinical presentation in 178 patients.

A retrospective analysis of clinical characteristics of 178 consecutive patients with extreme lateral lumbar disk herniation, amongst 3047 patients operated on for herniated lumbar disc, is presented. The level specific incidence of extreme lateral disc herniation (ELLDH) ranged from a low of 4.5% at L4-5 to peak of 17.4% at L3-4 although the largest number of ELLDH occurred at L4-5 and L5-S1 for a total number of 139 cases (78.1%). 43.6% of all L3 radiculopathies were caused by an L3-4 ELLDH, whereas only 4.4% of all L5 radiculopathies were caused by an L5-S1 ELLDH. Leg pain, either of the sciatic or the femoral type, was the first and dominant clinical symptom of radiculopathy, but pain radiation occurred not always in the appropriate dermatomal segment. ELLDH at upper levels (L2-3 and L3-4) caused usually none or only minor low back signs (76.2%), whereas ELLDH at lower levels more often caused moderate or major lumbar symptoms and signs (59.6%). Positive femoral nerve traction test with upper ELLDH showed a high frequency (84.4%) and reliability and is therefore an important clinical parameter in this situation. Motor deficits occurred more often (78.8%) than sensory deficits (46.6%), were usually of the monoradicular type and were therefore a more reliable clinical sign than sensory disturbances.

L4 nerve root exits at the L4-L5 foramina. L4 has a reflex assessed with a patellar reflex. When compressed by a herniated disc, it causes back pain that radiates into the anterior thigh and the medial aspect of the leg, accompanied with sensory loss in the same distribution, weakness in the hip flexion and adduction, weakness in knee extension, and a decreased patellar reflex.

Sciatica -- History and Physical

Another maneuver is the crossed straight leg test, similar to the straight leg raise test but is conducted on the asymptomatic leg instead. The crossed straight leg test is considered positive if the patient reports pain in the symptomatic leg while the asymptomatic leg is at a 40° angle, representing a central disc herniation with severe nerve root irritation. L3 radiculopathy includes weakness of hip adduction, knee extension, and sensory pain in the anteromedial dermatome of the thigh. Ankle dorsiflexion weakness and absent patellar reflex are present in L4 radiculopathy. Hip abduction and big toe extension weakness show L5 radiculopathy. S1 nerve root compression presents as absent ankle reflexes.

Disc Herniation -- History and Physical -- Physical Examination

L5 Nerve - back, radiating into buttock, lateral thigh, lateral calf, and dorsum foot, great toe; sensory loss on the lateral calf, dorsum of the foot, webspace between first and second toe; weakness on hip abduction, knee flexion, foot dorsiflexion, toe extension and flexion, foot inversion and eversion; decreased semitendinosus/semimembranosus reflex. S1 Nerve - back, radiating into buttock, lateral or posterior thigh, posterior calf, lateral or plantar foot; sensory loss on the posterior calf, lateral or plantar aspect of foot;  weakness on hip extension, knee flexion, plantar flexion of the foot; Achilles tendon; Medial buttock, perineal, and perianal region; weakness may be minimal, with urinary and fecal incontinence as well as sexual dysfunction. S2-S4 Nerves - sacral or buttock pain radiating into the posterior aspect of the leg or the perineum; sensory deficit on the medial buttock, perineal, and perianal region; absent bulbocavernosus, anal wink reflex.

InternalMed_Harrison

The straight leg–raising (SLR) maneuver is a simple bedside test for nerve root disease. With the patient supine, passive flexion of the extended leg at the hip stretches the L5 and S1 nerve roots and 113 CHAPTER 22 Back and Neck Pain 4th Lumbar vertebral body 5th Lumbar vertebral body 4th Lumbar pedicle L4 root Protruded L4-L5 disk L5 Root S1 Root S2 Root Protruded L5-S1 disk FIguRE 22-3 Compression of L5 and S1 roots by herniated disks. (From AH Ropper, MA Samuels: Adams and Victor’s Principles of Neurology, 9th ed. New York, McGraw-Hill, 2009; with permission.) the sciatic nerve. Passive dorsiflexion of the foot during the maneuver adds to the stretch. In healthy individuals, flexion to at least 80° is normally possible without causing pain, although a tight, stretching sensation in the hamstring muscles is common. The SLR test is positive if the maneuver reproduces the patient’s usual back or limb pain. Eliciting the SLR sign in both the supine and sitting positions can help

Lumbosacral Disc Injuries -- History and Physical

L5 at the L5/S1 level, a disc herniation far laterally into the left/right neural foramen would compress the L5 nerve, resulting in weakness of hip abduction muscles, ankle dorsiflexion (anterior tibialis muscle), and/or extension of the great toe (extensor hallucis longus muscle). S1 at the L5/S1 level, a disc herniation centrally into the canal would compress the S1 nerve, resulting in weakness of ankle plantar flexion (gastrocnemius muscle).

L1 nerve root exits at the L1-L2 foramina, assessed with a cremasteric reflex (male). When compressed by a herniated disc, it causes pain, and sensory loss in the inguinal region rarely causes weakness in the hip flexion. The L2 and L3 nerve roots exit at the L2-L3 and L3-L4 foramina, respectively. Symptoms worsen with sneezing, coughing, or leg straightening.

Intradural lumbar disc herniation associated with degenerative spine disease and rheumatoid arthritis.

A case report. To demonstrate a case of intradural lumbar disc herniation including imaging studies, intraoperative imaging, and an intraoperative video. The first case of lumbar intradural disc herniation was reported as early as 1942; since then more than 150 cases have been reported, mostly in the lumbar spine. Gadolinium-enhanced magnetic resonance image (MRI) is considered the "gold standard" for diagnosing this entity, although it is rarely performed routinely in lumbar disc disease and diagnosis is often made intraoperatively. A 70-year-old man presented to the emergency department as a referral complaining of lower back pain, loss of sensation in the right thigh, and difficulty walking. On examination, he showed uneven gait, right-sided foot drop (1/5), hypesthesias in the right inguinal area and ventral thigh, and a positive straight leg raise test on the right. Anal sphincter tone was within normal limits. A magnetic resonance image of the lumbar spine showed a large mediolateral herniated disc at L3-L4, with caudal displacement and unclear signal changes intradurally. Intraoperatively, the herniated disc was found upon opening the dural sac. Intradural disc herniations are a rare entity. The opening and inspection of the dural sack should be considered when the correct spinal level can be confirmed and insufficient herniated disc material can be visualized extradurally.

A careful and thorough neurological examination can help to localize the level of lumbar disc herniation if it is causing radiculopathy. The correct knowledge of the anatomy of nerve roots and lumbar disc herniations would allow a proper interpretation of the clinical findings associated with this condition. The radiculopathy associated with LDH varies based on the herniation type and the level at which the herniation occurred. In paracentral or lateral herniation, the transversing nerve root is usually affected; a lateral herniation at L4-L5 would cause L5 radiculopathy. Extreme lateral (far lateral) herniations typically result in the exiting nerve root being affected; extreme lateral herniation at L4-L5 would cause L4 radiculopathy.

A careful neurological examination can help in localizing the level of the compression. The sensory loss, weakness, pain location, and reflex loss associated with the different levels are described in Table 2. Table 2 . Typical findings of solitary nerve lesion due to compression by a herniated disc in the lumbar spine L1 Nerve - pain and sensory loss are common in the inguinal region. Hip flexion weakness is rare, and no stretch reflex is affected. L2-L3-L4 Nerves - back pain radiating into the anterior thigh and medial lower leg; sensory loss to the anterior thigh and sometimes medial lower leg; hip flexion and adduction weakness, knee extension weakness; decreased patellar reflex.

S1 nerve root exits at the S1-S2 foramina, assessed with the Achilles reflex. When compressed with a herniated disc, it presents with sacral or buttock pain that radiates into the posterolateral thigh, the calf, plantar or lateral foot or the perineum. Sensory loss is present on the calf, lateral, or plantar aspect of the foot. There is weakness on foot plantar flexion, hip extension, and flexion of the knee. Weakness in foot plantar flexion causes an inability to tiptoe walk. It could also cause urinary and fecal incontinence and sexual dysfunction. [5] [8] [9]

Intraradicular disc herniations in the lumbar spine and a new classification of intradural disc herniations.

A case report of intraradicular disc herniation. Intraradicular disc herniation is a special type of intradural disc herniations. In this report, we present the tenth case of intraradicular lumbar disc herniation and suggest a new classification for intradural disc herniations. A 32-year-old male was admitted to hospital having experienced pain in the lower back and right leg for 1 month prior to admission. Neurological examination revealed weakness of the extensor hallucis longus, positive Laségue's sign, decreased ankle reflex in his right lower extremity, and bilateral paravertebral muscle spasm. Magnetic resonance imaging (MRI) revealed a disc herniation with a posterolateral extruded fragment on the right at the level of the L5-S1 space. He underwent L5 laminectomy. During the operation, the right S1 root was found to be swollen and immobile. A longitudinal incision was made in the dura of the right S1 root and an intradural free disc fragment was removed, and the S1 root was relieved. The patient was free of pain postoperatively. We suggest a new classification for intradural disc herniations with this unusual case presentation and review the literature for pathogenesis, clinical picture, diagnosis and treatment.

InternalMed_Harrison

PART 2 Cardinal Manifestations and Presentation of Diseases FIguRE 22-1 Vertebral anatomy. (From A Gauthier Cornuelle, DH Gronefeld: Radiographic Anatomy Positioning. New York, McGraw-Hill, 1998; with permission.) Radicular pain is typically sharp and radiates from the low back to a leg within the territory of a nerve root (see “Lumbar Disk Disease,” below). Coughing, sneezing, or voluntary contraction of abdominal muscles (lifting heavy objects or straining at stool) may elicit the radiating pain. The pain may increase in postures that stretch the nerves and nerve roots. Sitting with the leg outstretched places traction on the sciatic nerve and L5 and S1 roots because the nerve passes posterior to the hip. The femoral nerve (L2, L3, and L4 roots) passes anterior to the hip and is not stretched by sitting. FIguRE 22-2 Spinal column. (From A Gauthier Cornuelle, DH Gronefeld: Radiographic Anatomy Positioning. New York, McGraw-Hill, 1998; with permission.)

Sciatica -- Differential Diagnosis -- Herniated Lumbosacral Disc

A careful and thorough neurological examination can help localize the level of lumbar disc herniation if causing radiculopathy. The radiculopathy associated with lumbar disc herniation varies based on the herniation type and the level at which the herniation occurred. In paracentral or lateral herniation, the transversing nerve root is usually affected. A lateral herniation at L4 to L5 would cause L5 radiculopathy. Extreme lateral (far lateral) herniations typically affect the exiting nerve root; far lateral herniation at L4 to L5 would cause L4 radiculopathy. A straight leg raise test at an angle lower than 70° suggests radiculopathies.

Pediatric lumbar disc herniation: a report of two cases and review of the literature.

Lumbar disc herniation (LDH) is not a common condition in children. Most reports on pediatric LDH concern the outcomes of surgeries performed in children in whom nonsurgical treatment failed while the outcome of nonsurgical treatment of LDH in children was rarely reported. Case 1: a 10-year-old girl presented with back pain and sciatica in her left leg for over 3 months. The physical examination revealed exacerbation of back pain by waist extension or flexion, and a positive Lasegue's sign was revealed in her left leg. Magnetic resonance imaging (MRI) revealed lumbar disc herniation at the L5/S1 level. She was diagnosed with LDH. After receiving nonsurgical treatment of traditional Chinese medicine (TCM) for 30 days, the girl had mild low back pain and sciatica and the symptoms had resolved completely at the 3-month follow-up. There was no recurrence within the following 2 years. MRI performed 30 months later revealed that the herniated disc did not shrink significantly. However, she was totally asymptomatic at the follow-up performed 30 months later. Case 2: a 13-year-old boy presented with sciatica in his left leg for over 3 months. The physical examination revealed that Lasegue's sign was positive in the left leg, the level of muscle strength in the left ankle plantar flexors was grade 4. MRI revealed a lumbar disc herniation at the L5/S1 level. He was diagnosed with LDH. The boy underwent 2 weeks of TCM treatment, and exhibited a favorable outcome: only mild pain was noticed in his left buttocks after walking for more than 15 min. He was asymptomatic at the 3-month follow-up and there was no recurrence within the next 3 years. MRI scan performed at 40 months later showed no significant resorption of the herniated disc. However, he was totally asymptomatic at the follow-up performed 40 months later. For the nonsurgical treatment of pediatric LDH, resorption of herniated discs is not necessary for favorable long-term outcomes, and children with symptomatic LDH may become asymptomatic without resorption.

Nerve root

Lower limb radiculopathies The cause is a herniated intervertebral disc, often on a single nerve root. The first sign of the nerve root sickness is usually lumbago, which usually occurs with periods of remission. The time to develop a full radicular syndrome may take several months or several years. Pain generally increases gradually, but it can also be sudden. Cold causes muscle contraction, which leads to increased previously hidden symptoms. Symptoms Scoliosis Paraspinal muscle contracture The reduction of lumbar lordosis Tingling or numbness Increased sensitivity Other inflammatory diseases L4 radiculopathy Pain located on the front of the thigh and shin further radiates towards the inner ankle, sometimes the medial toe Occasionally, failure of the quadriceps muscle and reflex weakness L5 radiculopathy Pain radiates to the side of the thigh and lower leg towards the back of the foot and toes 1–3 All reflexes are preserved

Percutaneous endoscopic lumbar discectomy: minimally invasive technique for multiple episodes of lumbar disc herniation.

Although open lumbar discectomy is a gold standard surgical technique for lumbar disc herniation (LDH), surgery-induced tissue injury may actually become a source of postsurgical pain. Percutaneous endoscopic lumbar discectomy (PELD) is introduced as a minimal invasive spinal technique for LDH. The PELD has gained popularity and shown successful results. The authors report the clinical usefulness of the PELD technique in two patients with the serial multilevel LDHs. A 32-year-old man suffered from radicular pain at the L5 dermatome due to the down migrated soft LDH at the L4-5 level. The PELD was performed to remove the ruptured fragments, yielding a complete decompression of the L5 nerve root. Four years later, he visited the clinic because of right leg radiating pain along the S1 dermatome. An MRI scan revealed the LDH at the L5-S1 level. The PELD with foraminoplasty was also performed successfully at the L5-S1 level. Two months after the second PELD, he visited the clinic again because of severe pain along the left L4 dermatome; consequently, the PELD was also performed at the L3-4 level without any complications. A 34-year-old man presented with radiating pain in the back and both legs at the L5 dermatome. The MR images show a disc extrusion at the L4-5. The patient underwent the PELD at the L4-5 via the left approach. After the PELD, the back and leg pain both improved. One year later, the patient suffered from severe pain in the back and the left anterior thigh. The MR images show a left paramedian LDH at the L2-3. After the PELD was performed at the L2-3, the pain was relieved. The final MR images show no signs of any aggravated degeneration of the intervertebral discs or the facet joints at all of the treated levels. When multiple episodes of LDH occur in a patient's life span, PELD could be considered as an alternative good technique to treat LDH in each step by preserving normal anatomic structures.

Total Resorption of a Chronic L4-L5 Disc Extrusion After Application of the Atlasprofilax Method: A Case Report.

BACKGROUND The intervertebral disc extrusion resorption has been described in the literature by various authors. It occurs in up to 75% of patients with symptomatic extruded lumbar discs. The Atlasprofilax method favors osteo-musculo-articular rehabilitation processes, mainly impacting on 2 levels: the first is the bone anatomy of the atlanto-occipital joint, and the second is the fasciae located in the cervical region. CASE REPORT A 42-year-old male patient diagnosed by MRI with dehydration of L2-L3 to L5-S1 intervertebral discs, disc bulging at L2-L3 and L3-L4, and disc extrusion at L4-L5, received a one-time neuromuscular treatment, called the Atlasprofilax method, to the suboccipital region. In a repeat MRI 6 months later, the disc extrusion at L4-L5 was totally resorbed and improvement in the L3-L4 and L4-L5 disc bulges was seen. The patient's symptoms prior to the Atlasprofilax treatment included bilateral trapezius pain, right brachialgia, constant chronic low back pain, right sciatica, gait claudication, and paresthesia and dysesthesias in the lower limbs with associated pain and numbness in the calves. These symptoms were ameliorated after the treatment. The sciatica disappeared 1 week after the treatment and did not recur. In a follow-up 5 years later, the remaining symptoms had improved even further. CONCLUSIONS We propose that alterations of the cervical musculature and deep fascia could predispose to the development of lumbar disc abnormalities. We therefore also propose that improvements in this patient, both in symptoms and in imaging findings, are due to a reduction of the asymmetric distribution of forces and elastic loading as a result of the Atlasprofilax treatment.

Neurology_Adams

The pain of herniated intervertebral disc varies in severity from a mild aching discomfort to severe knife-like stabs that radiate the length of the leg and are superimposed on a constant intense ache. Sciatic pain is perceived by the patient as originating deep in the buttock and radiating to the posterolateral thigh; it may progress to the calf and ankle—to the medial malleolus (L4), lateral malleolus (L5), or heel (S1). Distal radiation to the foot is infrequent and should raise concern of an alternative process. Abortive forms of sciatica may produce aching discomfort only in the lower buttock or proximal thigh and occasionally only in the lower hamstring or upper calf. With the most severe pain, the patient is forced to stay in bed, avoiding the slightest movement; a cough, sneeze, or strain is intolerable. The most comfortable position is lying on the back with legs flexed at the knees and hips and the shoulders raised on pillows to obliterate the lumbar lordosis. For some

Segmental lumbar rotation in patients with discogenic low back pain during functional weight-bearing activities.

Little information is available on vertebral motion in patients with discogenic low back pain under physiological conditions. We previously validated a combined dual fluoroscopic and magnetic resonance imaging system to investigate in vivo lumbar kinematics. The purpose of the present study was to characterize mechanical dysfunction among patients with confirmed discogenic low back pain, relative to asymptomatic controls without degenerative disc disease, by quantifying abnormal vertebral motion. Ten subjects were recruited for the present study. All patients had discogenic low back pain confirmed clinically and radiographically at L4-L5 and L5-S1. Motions were reproduced with use of the combined imaging technique during flexion-extension, left-to-right bending, and left-to-right twisting movements. From local coordinate systems at the end plates, relative motions of the cephalad vertebrae with respect to caudad vertebrae were calculated at each of the segments from L2 to S1. Range of motion of the primary rotations and coupled translations and rotations were determined. During all three movements, the greatest range of motion was observed at L3-L4. L3-L4 had significantly greater motion than L2-L3 with left-right bending and left-right twisting movements (p < 0.05). The least motion occurred at L5-S1 for all movements; the motion at this level was significantly smaller than that at L3-L4 (p < 0.05). Range of motion during left-right bending and left-right twisting at L3-L4 was significantly larger in the degenerative disc disease group than in the normal group. The range of motion at L4-L5 was significantly larger in the degenerative group than in the normal group during flexion; however, the ranges of motion in both groups were similar during left-to-right bending and left-to-right twisting. The greatest range of motion in patients with discogenic back pain was observed at L3-L4; this motion was greater than that in normal subjects, suggesting that superior adjacent levels developed segmental hypermobility prior to undergoing fusion. L5-S1 had the least motion, suggesting that segmental hypomobility ensues at this level in patients with discogenic low back pain.

[Electromyographical study of the straight leg raising test in lumbar disc herniation].

The straight leg raising test is one of the most reliable test for the diagnosis of the disc herniation. It is well known that the pain is produced by the increased tension of the affected root. However, the patient's response to the pain evoked by the straight leg raising test is not uniform. In some patients the leg is raised beyond the straight leg raising positive angle without resistance and some young patients show the tight hamstrings phenomenon. To elucidate these phenomena, the muscle action of erector spinae, gluteus maximus and biceps femoris evoked by this test was studied electromyographically. The results are as follows: 1) The muscle action patterns in the patients of disc herniation which are not observed in normal group are classified into four groups, namely LGB type (erector spinae, gluteus maximus and biceps femoris act), GB type (gluteus maximus and biceps femoris act), G type (gluteus maximus only acts), B type (biceps femoris only act). These abnormal muscle actions disappear under general anesthesia and are different from the actions which are recorded when the patients resist passive straight leg raising intentionally. 2) In the case of L4-5 intervertebral disc herniation mainly gluteus maximus acts as the resisting force against the passive straight leg raising. On the other hand, biceps femoris acts mainly in the case of L5-S1 disc herniation. 3) The group of younger age and less degenerated disc shows more resistance against straight leg raising and records the action potential of resisting muscles in earlier stage of the leg raising test.

Spinal Stenosis -- History and Physical

Stenosis in the lumbar spine can lead to neurogenic claudication, myeloradiculopathy symptoms, sensory disturbances, motor weakness, and pathologic reflexes. Patients will present with complaints of cramping pain in the leg, calf, and or buttocks. They might report an increase in pain with walking or standing for prolonged periods and relief when sitting or leaning forward while using a shopping cart. [9] Disk herniation is most common at the L4-5 and L5-S1 levels. A herniated disk at L5-S1 can lead to plantarflexion weakness, decrease sensation in the lateral foot, and cause pain in the posterior leg. A disk herniation at L4-5 can lead to a foot drop and numbness in the large toe web and dorsal aspect of the foot. Lastly, an L3-4 disk herniation can lead to knee extension weakness, numbness in the medial foot, and pain in the anterior thigh.

Successful Endoscopic Surgery for L5 Radiculopathy Caused by Far-Lateral Disc Herniation at L5-S1 and L5 Isthmic Grade 2 Spondylolisthesis in a Professional Baseball Player.

We report the case of a professional baseball player who had severe leg pain due to lumbar lateral disc herniation at L4-5 and isthmic spondylolisthesis at L5 (double crash syndrome). For early recovery to competitive level, we performed minimally invasive endoscopic decompression surgery without fusion. There are few reports to discuss the usefulness of minimally invasive treatment for top athletes. A 29-year-old professional baseball player who played catcher was referred to us with a complaint of right leg pain. The previous doctor diagnosed far-lateral disc herniation and Grade 2 isthmic spondylolisthesis and recommended arthrodesis at L5-S1 as treatment for both pathologies. Radiological imaging showed that the right L5 nerve root was impinged by the 2 lumbar disorders, namely, far-lateral disc herniation and a ragged edge around a pars defect. We had taken into account the patient's occupation and his wish to avoid a lengthy sick leave, and we had performed endoscopic decompression surgery during the offseason. The far-lateral disc herniation at L5-S1 was removed under local anesthesia by percutaneous endoscopic discectomy, after which the ragged edge at the pars defect was removed under general anesthesia using a microendoscopic discectomy system. Given that the patient did not have any low back pain, arthrodesis was not considered. The leg pain resolved after surgery. The following year (2015), the patient resumed playing baseball from the beginning of the season and played in 41 games. In the 2016 season, he played in 71 games without any symptoms. No further slippage was observed at radiological follow up 1 year after the surgery. Minimally invasive endoscopic surgery is an option for radiculopathy in very active patients who need an early return to their previous level of physical activity.

Back Pain -- History and Physical

Some provocative exercises can help provide clues about the cause of back pain. One is the straight-leg-raising (SLR) test, which is useful for diagnosing lumbar disk herniation. The test is performed by raising the patient’s leg to 30° to 70°. The result is positive if ipsilateral leg pain develops at less than 60°. A crossed SLR test raises the leg contralateral to the side of disk herniation. A positive crossed SLR test result is even more specific than a positive SLR test. [15] [16]

InternalMed_Harrison

Fever, constant pain uninfluenced by position, sphincter abnormali-115 ties, or signs of spinal cord disease suggest an etiology other than lumbar disk disease. Absence of ankle reflexes can be a normal finding in persons older than age 60 years or a sign of bilateral S1 radiculopathy. An absent deep tendon reflex or focal sensory loss may indicate injury to a nerve root, but other sites of injury along the nerve must also be considered. For example, an absent knee reflex may be due to a femoral neuropathy or an L4 nerve root injury. A loss of sensation over the foot and lateral lower calf may result from a peroneal or lateral sciatic neuropathy or an L5 nerve root injury. Focal muscle atrophy may reflect injury to the anterior horn cells of the spinal cord, a nerve root, peripheral nerve, or disuse.

A Novel Treatment Combination for Failed Back Surgery Syndrome, With a 41-Month Follow-Up: A Retrospective Case Report.

The purpose of this retrospective case report was to describe chiropractic management of a patient with failed back surgery syndrome. A 45-year-old woman presented 2 years after L4-L5 and L5-S1 fusion surgery with low back and sciatic pain. Her physical exam included a positive straight leg raise and diminished lower-extremity reflexes and muscle strength. The patient's magnetic resonance imaging showed right disc bulging and annular tearing at L2-L3 and L3-L4 disc bulging with foraminal impingement. A total of 52 treatments were provided over 28 weeks consisting of multidirectional functional decompression (FD) unweighted gait training, core exercises while in FD, strengthening exercises on a vibration platform, and supine spinal FD with vibration and chiropractic spinal manipulative therapy. Over the course of treatment, the patient noted gradual improvement in function (Oswestry Disability Index) and pain (Numeric Rating Scale), with a reduction in pain medications. Follow-up of 41 months posttreatment revealed an Oswestry Disability Index score of 0 and Numeric Rating Scale score of 0, and the patient no longer was using any pain medication. After a course of care, the patient in this study reported resolution of symptoms, decrease in pain medications, and improvement of function.

The contralateral (crossed) straight leg raise test: As in the straight leg raise test, the patient is lying supine, and the examiner elevates the asymptomatic leg. The test is positive if the maneuver reproduces the patient's typical pain and paresthesia. The test has a specificity higher than 90%.

Combined extraforaminal and intradiscal cement leakage following percutaneous vertebroplasty.

A case report and review of the literature are presented. To describe an extremely rare case of combined extraforaminal and intradiscal cement leakage in different vertebral levels following percutaneous vertebroplasty. Cement leaks in vertebroplasty are relatively common but generally not clinically significant. To our knowledge, this is the first report of extraforaminal cement leakage inducing radiculopathy combined with intradiscal cement leakage evoking acute adjacent compression fracture. A 78-year-old woman with L2 and L5 osteoporotic compression fractures received vertebroplasty. Two weeks after surgery, the patient presented severe low back pain radiating to the right thigh, with associated weakness and numbness in the right thigh and lower leg. Roentgenographic images revealed cement leakage into the right extraforamen of L2-L3 as well as leakage into L4-L5 disc with acute adjacent compression fracture of L4. Surgical intervention was required to relieve discomfort. One-stage posterior approach was performed: right L2-L3 intertransverse process approach with removal of extraforaminal leaked cement and posterior instrumentation from L3-L5 and posterior fusion. The severe low back pain, leg pain, and neurologic deficit associated weakness all improved after surgery. Although considered a minimally invasive procedure, percutaneous vertebroplasty with polymethylmethacrylate is not risk free. Intractable neurologic complications can occur if it is not performed by experienced physicians under appropriate indications and cautionary safeguards.