The most common symptomatology of a patient with coxarthrosis includes: hip pain that limits ambulation, nocturnal discomfort and even at rest, hip stiffness and locking. Coxo-femoral osteoarthrosis presents with a negative Lasegue test. Wrong answer 2. Low back pain of a neuropathic nature usually presents with unilateral and distributed radiculopathy according to dermatomes. The recognized risk factors are most frequently: women, obesity, smoking and sedentary lifestyle or situations of prolonged sitting. The lumbosciatica is usually referred to the buttock, posterior aspect of the thighs and even inguinal. The clinical case describes the Lasegue maneuver or test; a provocation test that evidences radicular irritation in the lumbosacral region (Answer 3 correct). Claudication due to canal stenosis typically presents with pain that worsens with trunk extension (walking, standing) and is relieved with flexion (sitting, sleeping in the fetal position...) Wrong answer 4.

The most common symptomatology of a patient with coxarthrosis includes: hip pain that limits ambulation, nocturnal discomfort and even at rest, hip stiffness and locking. Coxo-femoral osteoarthrosis presents with a negative Lasegue test. [HIDDEN]. Low back pain of a neuropathic nature usually presents with unilateral and distributed radiculopathy according to dermatomes. The recognized risk factors are most frequently: women, obesity, smoking and sedentary lifestyle or situations of prolonged sitting. The lumbosciatica is usually referred to the buttock, posterior aspect of the thighs and even inguinal. The clinical case describes the Lasegue maneuver or test; a provocation test that evidences radicular irritation in the lumbosacral region ([HIDDEN]). Claudication due to canal stenosis typically presents with pain that worsens with trunk extension (walking, standing) and is relieved with flexion (sitting, sleeping in the fetal position...) [HIDDEN].

A 61-year-old woman, administrative, with a history of overweight, hypertension, dyslipidemia and metabolic syndrome, who consults for pain in both buttocks, left trochanteric region, lateral aspect of the left thigh up to the knee and left leg up to the middle third. The pain appears when the lower limb is lifted with the knee extended, but is relieved when the knee is flexed. What is the first clinical suspicion?

Sacroiliac joint

Signs and symptoms The following are signs and symptoms that may be associated with an SI joint (SIJ) problem: Mechanical SIJ dysfunction usually causes a dull unilateral low back pain. The pain is often a mild to moderate ache around the dimple or posterior superior iliac spine (PSIS) region. The pain may become worse and sharp while doing activities such as standing up from a seated position or lifting the knee towards the chest during stair climbing. Pain is typically on one side or the other (unilateral PSIS pain), but the pain can occasionally be bilateral. When the pain of SIJ dysfunction is severe (which is infrequent), there can be referred pain into the hip, groin, and occasionally down the leg, but rarely does the pain radiate below the knee. Pain can be referred from the SIJ down into the buttock or back of the thigh, and rarely to the foot. Low back pain and stiffness, often unilateral, that often increases with prolonged sitting or prolonged walking.

Greater trochanteric pain syndrome

More often the lateral hip pain is caused by disease of the gluteal tendons that secondarily inflames the bursa. This is most common in middle-aged women and is associated with a chronic and debilitating pain which does not respond to conservative treatment. Other causes of trochanteric bursitis include uneven leg length, iliotibial band syndrome, and weakness of the hip abductor muscles. Greater trochanteric pain syndrome can remain incorrectly diagnosed for years, because it shares the same pattern of pain with many other musculoskeletal conditions. Thus people with this condition may be labeled malingerers, or may undergo many ineffective treatments due to misdiagnosis. It may also coexist with low back pain, arthritis, and obesity. Signs and symptoms The primary symptom is hip pain, especially hip pain on the outer (lateral) side of the joint. This pain may appear when the affected person is walking or lying down on that side. Diagnosis

Sciatica -- History and Physical

Further, a straight leg raise (SLR) test is a neurological maneuver performed while examining a patient presenting with lower back pain. This test is conducted with the patient lying supine while keeping the symptomatic leg straight by flexing the quadriceps. The examiner elevates the leg progressively at a slow pace. The test is deemed positive if it reproduces the patient's symptoms (pain and paresthesia) at an angle lower than 70° with radiation below the knee (Lasegue sign). This test is most helpful in diagnosing L4, L5, and S1 radiculopathies. The patient is asked to dorsiflex the foot while the examiner raises the leg (Bragaad sign) to increase the test's sensitivity. When executing the straight leg raise test, the examiner will slightly bend the patient's knee by 20° to 30°, which will lessen the pain. Then, manual pressure is applied in the popliteal fossa. The Bowstring sign is considered positive if it causes the same level of discomfort that the patient feels during a straight leg raise. [8] The Naffziger test involves reproducing pain via coughing. [9]

The piriformis muscle syndrome: a simple diagnostic maneuver.

Current maneuvers to diagnose the piriformis syndrome are less than ideal. Freiberg's maneuver of forceful internal rotation of the extended thigh elicits buttock pain by stretching the piriformis muscle, and Pace's maneuver elicits pain by having the patient abduct the legs in the seated position, which causes a contraction of the piriformis muscle. This report describes a maneuver performed by the patient lying with the painful side up, the painful leg flexed, and the knee resting on the table. Buttock pain is produced when the patient lifts and holds the knee several inches off the table. The maneuver produced deep buttock pain in three patients with piriformis syndrome. In 100 consecutive patients with surgically documented herniated lumbar discs, the maneuver often produced lumbar and leg pain but not deep buttock pain. In 27 patients with primary hip abnormalities, pain was often produced in the trochanteric area but not in the buttock. The maneuver described in this report was helpful in diagnosing the piriformis syndrome. It relies on contraction of the muscle, rather than stretching, which the author believes better reproduces the actual syndrome.

Sciatica -- History and Physical

A straight-leg raise has variable sensitivity and specificity and may or may not be present depending on the underlying cause. The straight-leg test is a passive examination where the patient first lies in a relaxed, supine position. The examiner then lifts the leg from the posterior aspect, flexing at the hip joint and keeping the knee in full extension or keeping the leg straight. Typically, pain that is reproduced between 30° to 70° of hip flexion and experienced primarily in the back is likely due to a lumbar disc herniation. Pain and parenthesis felt in the leg are possible due to lateralizing compression of a peripheral nerve. While not absolute, musculoskeletal causes of the pain usually reproduce pain above 70° of flexion and below 30° of flexion.

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.

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.

[Diagnosis and treatment of lumbar spinal canal stenosis].

Lumbar spinal canal stenosis (LSCS) was first described in 1954 by Verbiest, followed by the currently accepted international classification of LSCS in 1976 by Arnoldi. Briefly, LSCS is a nervous system syndrome that is characterized by neural symptoms in the lower extremities due to tightened cauda equina and spinal nerve root involvement. LSCS international classification consists of: (1) degenerative, (2) congenital developmental, (3) combined, (4) spondylolytic spondylolisthesis, (5) iatrogenic and (6) post traumatic stenosis. Degenerative stenosis-the most common type of LSCS-is caused by disc degeneration, osteoarthritis of the facet joint and hypertrophy of the ligamentum flavum. LSCS may also be the result of intervertebral disc degeneration, protruded intervertebral disc and/or bony spur compress cauda equina and spinal nerve root anteriorally, while degenerated facet joint and hypertrophied the ligamentum flavum compress cauda equina and spinal nerve root posteriorally? Most often, spondylolytic spondylolisthesis occurs at the fourth lumbar vertebrae in middle-aged women. As a result of a slipping forward of the vertebra, cauda equina and spinal nerve roots can be tightened between the edge behind the top of lower vertebra and frontal edge of the lower part of upper lamina. Typical clinical symptoms of LSCS are low back pain, leg pain and intermittent claudication. Low back pain is chronic with secondary radiating pain in the buttock. The leg pain is called "sciatica", which tends to appear on the back of thigh, in the lateral aspect of lower leg and calf muscles, and which intensifies when the patient is fatigued. Intermittent claudication is a symptom associated with this syndrome. Often, patients with LSCS find it impossible to walk because of increased numbness and pain in their leg. Many patients report that after squatting for a few minutes they are able to resume walking. LSCS patients may also report dysaesthesia in the perineum area, and may also report urinary dysfunction ranging from extreme urgency to urinary delay. Patients who present with symptoms of LSCS should be seen by an orthopedic surgeon. Correct diagnosis by imaging and clinical examination, with appropriate conservative or operative treatment in a timely fashion should be encouraged in order to prevent irreversible nerve damage.

Low back pain

Low back pain may be classified based on the signs and symptoms. Diffuse pain that does not change in response to particular movements, and is localized to the lower back without radiating beyond the buttocks, is classified as nonspecific, the most common classification. Pain that radiates down the leg below the knee, is located on one side (in the case of disc herniation), or is on both sides (in spinal stenosis), and changes in severity in response to certain positions or maneuvers is radicular, making up 7% of cases. Pain that is accompanied by red flags such as trauma, fever, a history of cancer or significant muscle weakness may indicate a more serious underlying problem and is classified as needing urgent or specialized attention.

GALS screen

Now ask the patient to do the following noting any painful, restricted or asymmetrical movements: Test rotation of the thoracic and lumbar spine. Gently hold the patient's hips still and ask them to: "Turn your shoulders round as far as you can to the left, then do the same to the right." Test lateral flexion of the thoracic and lumbar spine: "Stand up straight and then slide the palm of your right hand down your thigh towards your knee, bending your shoulder down to the side." "Now do the same with your left hand down your left leg." "Bend your left ear down towards your left shoulder and then your right ear down towards your right shoulder" to test for pain free cervical spine lateral flexion. Now test for stiffness or pain flexing or extending the cervical spine: "bend your neck forwards to try to touch your chin against your chest." "bend your neck back to lift your chin."

Greater trochanteric pain syndrome: a review of anatomy, diagnosis and treatment.

Greater trochanteric pain syndrome (GTPS) is a term used to describe chronic pain overlying the lateral aspect of the hip. This regional pain syndrome, once described as trochanteric bursitis, often mimics pain generated from other sources, including, but not limited to myofascial pain, degenerative joint disease, and spinal pathology. The incidence of greater trochanteric pain is reported to be approximately 1.8 patients per 1000 per year with the prevalence being higher in women, and patients with coexisting low back pain, osteoarthritis, iliotibial band tenderness, and obesity. Symptoms of GTPS consist of persistent pain in the lateral hip radiating along the lateral aspect of the thigh to the knee and occasionally below the knee and/or buttock. Physical examination reveals point tenderness in the posterolateral area of the greater trochanter. Most cases of GTPS are self-limited with conservative measures, such as physical therapy, weight loss, nonsteroidal antiinflammatory drugs and behavior modification, providing resolution of symptoms. Other treatment modalities include bursa or lateral hip injections performed with corticosteroid and local anesthetic. More invasive surgical interventions have anecdotally been reported to provide pain relief when conservative treatment modalities fail.

Lumbosacral Facet Syndrome -- History and Physical

In most presentations, facetogenic lumbosacral pain often presents secondary to chronic pain alone. It should, however, be noted that facet joint pain may be referred distally into the lower limb, thus mimicking sciatica. In these cases of "pseudo-radicular" lumbar pain, patients typically experience radiation into the unilateral or bilateral buttocks and the trochanteric region (from L4 and L5 levels), the groin and thighs (from L2 to L5), ending above the knee, and without any neurologic deficits. At times, pain may radiate further down the lower extremity reaching the foot, thus mimicking sciatic pain. This may occur especially in the setting of rather large synovial cysts causing direct mechanical compression and creating ensuing inflammation to further irritate the surrounding nerve roots. [15] Facet joint pain is typically worse in the mornings and following periods of inactivity. Stress exercise, lumbar spinal extension or rotary motions, standing or sitting positions, and facet joint palpation may also elicit lumbar facetogenic pain. [2]

Radicular Back Pain -- History and Physical

L2, L3, and L4 lumbar radiculopathies are considered a group. This group has a marked overlap of the innervation of the anterior thigh muscles. [1] An acute injury in the distribution of L2, L3, and L4 will most commonly present with the patient experiencing radiating back pain to the anterior aspect of the thigh, which may progress into their knee, and possibly radiate to the medial aspect of the lower leg, into the foot. On examination, patients can have weakness during knee extension, hip adduction, and or hip flexion. There is often a loss of sensation over the anterior thigh along the area of pain. The patient may show a reduced patellar reflex (L4). [1] Activities that can make the symptoms worse include coughing, leg straightening, or sneezing.

InternalMed_Harrison

2692 LATERAL FEMORAL CUTANEOUS NEUROPATHY (MERALGIA PARESTHETICA) The lateral femoral cutaneous nerve arises from the upper lumbar plexus (spinal levels L2/3), crosses through the inguinal ligament near its attachment to the iliac bone, and supplies sensation to the anterior lateral thigh. The neuropathy affecting this nerve is also known as meralgia paresthetica. Symptoms and signs consist of paresthesias, numbness, and occasionally pain in the lateral thigh. Symptoms are increased by standing or walking and are relieved by sitting. There is normal strength, and knee reflexes are intact. The diagnosis is clinical, and further tests usually are not performed. EDx is only needed to rule out lumbar plexopathy, radiculopathy, or femoral neuropathy. If the symptoms and signs are classic, EMG is not necessary. Symptoms often resolve spontaneously over weeks or months, but the patient may be left with permanent numbness. Treatment consists of weight loss and avoiding tight belts. Analgesics

Greater Trochanteric Pain Syndrome -- History and Physical

Patients with greater trochanteric pain syndrome usually have lateral hip pain, tenderness over and around the greater trochanter, pain at end-range hip rotation, abduction or adduction, pain with resisted hip abduction, and a positive Patrick-FABER (flexion abduction external rotation) test. Patients usually suffer from chronic back pain radiating to the posterolateral aspect of the thigh, leg paresthesias, and tenderness over the iliotibial tract. [6] They will often complain of the inability to lay on the affected hip. The mean duration of symptoms before treatment ranges from 7.1 weeks to 4.4 years. Young adults (18 to 35 years old) with hip pain often present with non-specific symptoms and vague findings from the history and physical examination, which may lead to a misdiagnosis of GTPS or trochanteric bursitis. [1] [4]

Neurology_Adams

The most characteristic syndrome affects the lumbar roots. Pain, which can be severe, begins in the low back or hip and spreads to the thigh and knee on one side; the discomfort has a deep, aching character with superimposed lancinating jabs and there is a propensity for pain to be most severe at night. Weakness and later atrophy are evident in the pelvic girdle and thigh muscles, although the distal muscles of the leg may also be affected. The weakness can progress for days or weeks (rarely, months). The patellar reflex is lost on the affected side. Curiously, we have found the opposite patellar reflex to be absent in some patients, without explanation. Deep and superficial sensation may be intact or mildly impaired, conforming to either a multiple nerve or multiple adjacent root distribution (i.e., L2 and L3, or L4 and L5). The pain lasts for several days and then gradually abates. Motor recovery is the rule although months and even years may elapse before it is complete. The same

Surgery_Schwartz

heavy-muscled athletesVenous claudicationEntire leg, but usually worse in thigh and groinTight, bursting painAfter walkingSubsides slowlyRelief speeded by elevationHistory of iliofemoral deep venous thrombosis, signs of venous congestion, edemaNerve root compression (e.g., herniated disk)Radiates down leg, usually posteriorlySharp lancinating painSoon, if not immediately after onsetNot quickly relieved (also often present at rest)Relief may be aided by adjusting back positionHistory of back problemsSymptomatic Baker’s cystBehind knee, down calfSwelling, soreness, tendernessWith exercisePresent at restNoneNot intermittentIntermittent claudication (hip, thigh, buttock)Hip, thigh, buttocksAching discomfort, weaknessAfter same degree of exerciseQuickly relievedNoneReproducibleHip arthritisHip, thigh, buttocksAching discomfortAfter variable degree of exerciseNot quickly relieved (and may be present at rest)More comfortable sitting, weight taken off legsVariable, may relate to activity

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.

Spinal gouty tophus presenting as an epidural mass lesion - A case report.

Gout is a metabolic disease secondary to an increased body pool of urate with hyperuricemia. Gout typically affects the peripheral joints and rarely involves the intra-spinal area. A 43-year-old man, who had metabolic syndrome s/p bariatric surgery and gout suffered from severe left low back pain with radiation to the lateral side of his left thigh and anterior side of his left leg for more than 7 days. His L-spine MRI showed an abnormal posterior epidural space occupying lesion at L4-L5 level. For tissue diagnosis and neural structures decompression, he underwent surgical removal of the epidural mass lesion. The surgical specimen showed a picture of gout and he got a good recovery after operation. The differential diagnoses of an epidural mass includes synovial cysts, ligament cyst, cystic neuromas, tumors, hematomas and abscesses. Gout in the spinal canal is difficult to diagnosis before surgery because it is rare and its clinical presentation and radiologic findings mimic tumor, abscess, tuberculosis, and degenerative spinal diseases. Patients with spinal gout may present with axial pain and a variety of neurological symptoms. Spinal gouty tophus should be considered in the different diagnoses of spinal epidural masses especially in patients with systemic gout. Surgery is needed for final diagnosis. If spinal gouty tophus is highly suspected during the surgery, the specimen should not be preserved with Formalin because birefringent crystals under polarized light is a unique feature for gouty tophus but they dissolve in Formalin.

[Acromegaly and spinal canal stenosis].

A rare case of acromegaly with radiculomyelopathy due to spinal canal stenosis is reported. A long history of acromegalic deformity was seen on this 55 years old acupuncture therapist for the last 18 years, while he had developed unusually increased appetite, profuse perspiration and gained weight. Fifteen years ago, acromegalic tendency became prominent and was accompanied by low back and knee pain. In 1974 CB-154 was administered in several occasions beside 4000 rads irradiation to the sella. After radiation therapy was completed his outlook was somewhat improved, although low back pain was aggravated and associated with atrophy of the left lower extremity. The neurological examination at admission in 1980 revealed acromegalic feature, increased DTRs on both upper and lower extremities, dysesthesia of feet and atrophy of the leg muscles in general, mainly due to diffuse atrophy. Patient bended knees due to pain and unable to walk. He had radiating pain in the postero-lateral aspect of the left lower extremity and some dysesthesia of feet, although no specific root lesion was identifiable. Spinal roentgenograms disclosed diffuse ossification of anterior and posterior longitudinal ligaments, and marked spondylotic changes. Although the low back pain was impending complaint of the patient, the hypophyseal tumor was advised to remove and transsphenoidal hypophyseal adenomectomy was performed. A good amount of softend tumor tissue was removed however, adenoma found markedly fibrotic. Low back pain and knee were decreased gradually, but intermittent claudication was evident. Acromegaly in association with spinal canal stenosis were reviewed in literature, and the relationship of growth hormone and therapeutic problems were discussed.

A straight leg raising can be helpful in lumbosacral radiculopathy. The mechanism of pain during a straight leg raise is increased dural tension placed upon the lumbosacral spine during the test. Patients lay supine during the test. The physician will flex the patient's quadriceps with the leg in extension as well as dorsiflex the patient's foot on the symptomatic side. Pain or reproduction of paresthesias is considered a positive test (Lasegue's sign). A Bowstring sign relieves this underlying radicular pain with flexion of the patient's knee on the affected side. The straight leg raising test is most helpful in the diagnosis of L4 and S1 radiculopathies. [11] [3]

Diabetic amyotrophy, not your typical back pain.

A 49-year-old man presented to the hospital for spinal cord decompression surgery with left buttock and left leg pain. The patient described an acute burning pain radiating down from his left buttock to left lateral leg. He also noted a 13.6 kg weight loss in recent months. Physical examination showed decreased muscle bulk of the left thigh, decreased strength of the left hip, left knee flexors and extensors. Recent MRI spine showed mild canal narrowing and cord flattening in the lower thoracic spine. Serologic testing showed an elevated glucose of 17.9 mmol/L and haemoglobin A1c of 9.8%. Electromyography showed denervation of scattered muscles of the left knee flexors, hip flexors and adductors. In the setting of newly diagnosed diabetes mellitus, he was diagnosed with diabetic amyotrophy, started on insulin therapy, and his surgery was cancelled.

Comparison of the history and physical examination for hip osteoarthritis and lumbar spinal stenosis.

Leg pain associated with walking is sometimes incorrectly attributed to hip osteoarthritis (OA) or lumbar spinal stenosis (LSS). This study compared physicians' values of signs and symptoms for diagnosing and differentiating hip OA and LSS to their clinical utility. Musculoskeletal physicians were surveyed with online questionnaires. Patients were recruited from hip and spine specialty practices. Seventy-seven hip OA and 79 LSS patients. Signs and symptoms of hip OA and LSS. Fifty-one of 66 invited musculoskeletal physicians completed online surveys about the values of 83 signs and symptoms for diagnosing hip OA and LSS. Of these, the most valued 32 symptoms and 13 physical examination items were applied to patients with symptomatic hip OA or LSS. Positive likelihood ratios (+LR) were calculated for each items' ability to differentiate hip OA from LSS, with a +LR>2 set as indicating usefulness for favoring either diagnosis. Positive LRs were compared with surveyed physicians' values for each test. All symptoms were reported by some patients with each diagnosis. Only 11 of 32 physician-valued symptoms were useful for discriminating hip OA from LSS. Eight symptoms favored hip OA over LSS: groin pain (+LR=4.9); knee pain (+LR=2.2); pain that decreased with continued walking (+LR=3.9); pain that occurs immediately with walking (+LR=2.4); pain that occurs immediately with standing (+LR=2.1); pain getting in/out of a car (+LR=3.3); pain with dressing the symptomatic leg (+LR=3.1); and difficulty reaching the foot of the symptomatic leg while dressing (+LR=2.3). Three symptoms favored LSS over hip OA: pain below the knee (+LR=2.3); leg tingling and/or numbness (+LR=2.7); and some pain in both legs (+LR=2.5). Notable symptoms that did not discriminate hip OA from LSS included: pain is less while pushing a shopping cart (+LR=1.0); back pain (+LR=1.1); weakness and/or heaviness of leg (+LR=1.1); buttocks pain (+LR=1.2); poor balance or unsteadiness (+LR=1.2); pain that increased with weight-bearing on the painful leg (+LR=1.3), and step to gait on stairs (+LR=1.7). Consistent with physicians' expectations, 7 of 13 physical examination items strongly favored hip OA over LSS: limited weight-bearing on painful leg when standing (+LR=10); observed limp (+LR=9); and painful and restricted range-of-motion with any of five hip maneuvers (+LR range 21-99). Four of five tested neurological deficits (+LR range 3-8) favored the diagnosis of LSS over hip OA. There is substantial crossover of symptoms between hip OA and LSS, with some physician-valued symptoms useful for differentiating these disorders whereas others were not. Physicians recognize the value of the examination of gait, the hip, and lower extremity neurological function for differentiating hip OA from LSS. These tests should be routinely performed on all patients for which either diagnosis is considered. Awareness of these findings might reduce diagnostic errors.

Pudendal tumor mimicking cauda equina syndrome and acute radiculopathy: case report.

Cauda equina syndrome (CES) is most caused by lumbar disc herniation, and the associated treatment involves prompt surgical decompression. Rarer causes of CES include perineural (Tarlov) cysts. A 62-year-old female with history of rheumatoid arthritis, hip and knee replacements, and chronic low back pain presented with worsening back pain, left leg weakness and pain for 6 weeks, and bowel/bladder incontinence with diminished sensation in the perianal region for 24 h prior to presentation. MRI demonstrated severe spinal stenosis at L4-S1, central disc herniation at L5-S1, and compression of the cauda equina, consistent with CES. A lumbar decompression was performed. Patient did well at 2-week follow up, but presented 5 weeks post-discharge with increased left leg pain/weakness and genitalia anesthesia. Imaging was unremarkable. Two months later, the patient presented with diminished sensation in the buttocks and bilateral lower extremities and bowel/bladder incontinence. Imaging demonstrated a large cystic presacral mass with involvement of the left sciatic foramen and S3 neural foramen. A team of plastic, orthopedic, and neurological surgeons performed an S3 sacral laminectomy, foraminotomy, partial sacrectomy, and S3 rhizotomy, and excision of the large left hemorrhagic pudendal mass. Final pathology demonstrated a perineural cyst with organizing hemorrhage. On follow-up, the patient's pain and weakness improved. CES-like symptoms were initially attributed to a herniated disk. However, lumbar decompression did not resolve symptoms, prompting further radiographic evaluation at two separate presentations. This represents the first reported case of a pudendal tumor causing symptoms initially attributed to a herniated disc.

Does this older adult with lower extremity pain have the clinical syndrome of lumbar spinal stenosis?

The clinical syndrome of lumbar spinal stenosis (LSS) is a common diagnosis in older adults presenting with lower extremity pain. To systematically review the accuracy of the clinical examination for the diagnosis of the clinical syndrome of LSS. MEDLINE, EMBASE, and CINAHL searches of articles published from January 1966 to September 2010. Studies were included if they contained adequate data on the accuracy of the history and physical examination for diagnosing the clinical syndrome of LSS, using a reference standard of expert opinion with radiographic or anatomic confirmation. Two authors independently reviewed each study to determine eligibility, extract data, and appraise levels of evidence. Four studies evaluating 741 patients were identified. Among patients with lower extremity pain, the likelihood of the clinical syndrome of LSS was increased for individuals older than 70 years (likelihood ratio [LR], 2.0; 95% confidence interval [CI], 1.6-2.5), and was decreased for those younger than 60 years (LR, 0.40; 95% CI, 0.29-0.57). The most useful symptoms for increasing the likelihood of the clinical syndrome of LSS were having no pain when seated (LR, 7.4; 95% CI, 1.9-30), improvement of symptoms when bending forward (LR, 6.4; 95% CI, 4.1-9.9), the presence of bilateral buttock or leg pain (LR, 6.3; 95% CI, 3.1-13), and neurogenic claudication (LR, 3.7; 95% CI, 2.9-4.8). Absence of neurogenic claudication (LR, 0.23; 95% CI, 0.17-0.31) decreased the likelihood of the diagnosis. A wide-based gait (LR, 13; 95% CI, 1.9-95) and abnormal Romberg test result (LR, 4.2; 95% CI, 1.4-13) increased the likelihood of the clinical syndrome of LSS. A score of 7 or higher on a diagnostic support tool including history and examination findings increased the likelihood of the clinical syndrome of LSS (LR, 3.3; 95% CI, 2.7-4.0), while a score lower than 7 made the diagnosis much less likely (LR, 0.10; 95% CI, 0.06-0.16). The diagnosis of the clinical syndrome of LSS requires the appropriate clinical picture and radiographic findings. Absence of pain when seated and improvement of symptoms when bending forward are the most useful individual findings. Combinations of findings are most useful for identifying patients who are unlikely to have the diagnosis.

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.

Bilateral periprosthetic stress fractures in a juvenile chronic arthritis patient secondary to bilateral genu valgum.

Lateral insufficiency fractures following total hip replacement have been reported with the femoral stems positioned in varus, together with osteopenia of the lateral femoral cortex. Any abnormal alignment of the lower limbs, such as genu valgum, will alter the load distribution across the femoral cortices, and repetitive loading during walking will predispose the bones to stress fractures at any stress riser point, such as the tip of a femoral component. Bilateral femoral stress fractures post total hip replacements have not been previously described. We present a 55-year-old woman, diagnosed with juvenile idiopathic arthritis, who had undergone bilateral total hip replacements and bilateral knee replacements. The knees 15 years postoperatively were in valgus and the left knee was extremely stiff, flexing to just 5. The patient presented with bilateral thigh pain, with plain radiographs confirming bilateral periprosthetic fractures of the femur at the tip of well-fixed femoral components. There was no history of injury and her hips were functioning well up to this time. The patient required revision of both hips to long-stem uncemented components, bypassing the fractures, and revision of both knees to stemmed semi-constrained implants, thereby correcting the alignment of both lower limbs. Both fractures healed and the patient is currently pain-free and mobile with walking aids. Surgeons must remain aware that when implants are in situ, abnormal alignments will lead to abnormal forces, and stress fractures are likely to occur at any stress riser around the implant. Avoiding malalignment will avoid this complication.

Plantar Heel Pain -- History and Physical -- S1 Radiculopathy

Patients with heel pain may have a history of chronic lower back pain. Clinically, radicular involvement will present as pain and numbness radiating from the lower back down to the heel of the foot. Patients may have decreased sensation over the skin of the sole, heel, or lateral foot and weakness of the gastrocnemius, gluteus maximus, hamstring, peroneal, and foot muscles with a diminished ankle reflex. Perform the positive straight leg raise test (Lasègue test) with the patient in the supine position. Pain with passive hip flexion while lifting the leg suggests stretching the lower lumbar and sacral roots. [21] Perform a crossed straight leg raise test, eliciting pain on the contralateral side with the same motion. Results from new studies suggest that these exams may not be as reliable as we once thought. [22]

Neurogenic claudication

Knee to chest stretch - Laying down on the back, bring one leg up and pull it towards the chest and hold for 30–45 seconds. Posterior pelvic tilt (bridges) - Laying on the back, bend both legs and place your feet on the floor. Raise stomach from the ground, lifting the back and pelvis, until the back is straight. Hold for 5–10 seconds and relax. Neural Stretching of the legs - Laying on the back, bring one leg up with a stretching band until a stretch is felt in the legs. Ensure your legs are straight. Once the stretch is felt, hold for 30–45 seconds and relax. Hip-flexor stretch - To stretch the right hip-flexor, bring the left leg forward, and kneel on the right knee. Push the pelvis forward (lean forward), whilst keeping the upper body straight. Hold the position for 30–45 seconds and relax. To stretch the left hip-flexor, bring swap the positions of the legs.

Deep vein thrombosis in an athletic military cadet.

Resident's case problem. A 21-year-old healthy athletic male military cadet with complaint of worsening diffuse left knee pain was evaluated 4 days after onset. The knee pain began 2 hours after completing a long car trip, worsened over the subsequent 3 days, and became almost unbearable during the return trip. The patient reported constant pain, limited knee motion, and difficulty ambulating. In addition, he was unable to perform physical military training or attend academic classes due to the severe left knee pain. Past medical history revealed a mild left lateral calf strain 21/2 weeks prior, which completely resolved within 24 hours of onset. Our physical examination led us to either monoarticular arthritis, pseudothrombophlebitis (ruptured Baker's cyst), or a lower leg deep vein thrombosis (DVT) as the cause of knee pain. Diagnostic imaging of this patient revealed a left superficial femoral vein thrombosis and popliteal DVT, with bilateral pulmonary emboli (PE). A systematic differential diagnosis was undertaken to rule out a potentially fatal DVT diagnosis as the cause of knee pain, despite minimal DVT risk factors. The physical therapist in a direct-access setting must ensure timely evaluation and referral of a suspected DVT, even when patient demographics cause the practitioner to question the likelihood of this diagnosis. The physical examination findings, clinical suspicion, and established clinical prediction rules can accurately dictate the appropriate referral action necessary.

What was the disease of the legs that afflicted King Asa?

The elderly have suffered from pain in their legs, which may be associated with various diseases, for thousands of years. This report analyzes the disease that afflicted the biblical King Asa (the third king of the house of Judah who reigned between 867 and 906 BCE). The sentence 'Nevertheless in the time of his old age he was diseased in his legs' indicates that King Asa suffered from disease in his legs. Among numerous diseases, peripheral vascular disease, gout, and degenerative osteoarthritis were most likely to affect the King's legs. And among these diseases, the diagnosis of peripheral vascular disease is the most acceptable. This report shows that the roots of contemporary modern gerontology can be traced back to biblical times.

Multiple Venous Thromboses Presenting as Mechanical Low Back Pain in an 18-Year-Old Woman.

The purpose of this case report is to describe a patient who presented with acute musculoskeletal symptoms but was later diagnosed with multiple deep vein thrombosis (DVT). An 18-year-old female presented to a chiropractic clinic with left lumbosacral pain with referral into the posterior left thigh. A provisional diagnosis was made of acute myofascial syndrome of the left piriformis and gluteus medius muscles. The patient received 3 chiropractic treatments over 1 week resulting in 80% improvement in pain intensity. Two days later, a sudden onset of severe abdominal pain caused the patient to seek urgent medical attention. A diagnostic ultrasound of the abdomen and pelvis were performed and interpreted as normal. Following this, the patient reported increased pain in her left leg. Evaluation revealed edema of the left calf and decreased left lower limb sensation. A venous Doppler ultrasound was ordered. Doppler ultrasound revealed reduction of the venous flow in the femoral vein area. An additional ultrasonography evaluation revealed an extensive DVTs affecting the left femoral vein and iliac axis extending towards the vena cava. Upon follow-up with a hematologist, the potential diagnosis of May-Thurner syndrome was considered based on the absence of blood dyscrasias and sustained anatomical changes found in the left common iliac vein at its junction with the right common iliac artery. A week following discharge, she presented with chest pain and was diagnosed with venous thromboembolism. The patient was successfully treated with anticoagulation therapy and insertion of a vena cava filter. Although DVTs are common in the general population, presence in low-risk individuals may be overlooked. In the presence of subtle initial clinical signs such as those described in this case report, clinicians should keep a high index of suspicion for a DVT. Rapid identification of such clinical signs in association with a lack of objective examination findings warrants further evaluation due to potentially negative outcomes.


It is a semiology question that helps us to remember the types of aphasia. The following aspects should be taken into account: language emission (fluent, non-fluent, non-emission), comprehension (yes or no), repetition (yes or no) and nomination. Wernicke's aphasia or sensitive aphasia has a fluent language, does not understand, does not repeat and does not nominate, just like the patient in the question. Sensory transcortical aphasia differs from sensory aphasia in that patients are able to repeat. Conduction aphasia differs from sensory aphasia in that comprehension is preserved, all else being equal. Finally, in broca's aphasia the language is non-fluent, comprehension is preserved, it does not repeat and does not nominate.

An 80-year-old woman with a history of arterial hypertension and diabetes mellitus who suddenly presents with language impairment. On arrival at the hospital, an unknown atrial fibrillation is observed, and on examination she presents fluent speech with a tendency to slurred speech, poor language comprehension, inability to repeat and dysnomia. Semiologically she presents a picture compatible with:

[Crossed aphasia in right-handed patients. II. Neuropsychological and neurolinguistic study of a case. Evolution over a 2 year period].

We present an unusual case of crossed aphasia in a doctor who is totally right handed, following an infarction which almost completely destroyed his right hemisphere. The observations--linguistic and extra linguistic--during a study over two years are presented. The aphasia evolved in three stages, taking semiological and evolutive aspects not commonly met with. In speech and writing there were: 1. an oral agrammatism and a written dyssyntaxia in the initial stage; 2. the evolution of a non-fluent speech typically agrammatic leading to a jargonaphasia; 3. a dissociation between oral and written language, characterised by phonemic paraphasias in speech and dyssyntaxia in writing. Comprehension was good except for a verbal class called "empty signs" of language, in which the lexic which refers to the notion of space and time has a primary role. On an extra linguistic level some of the usual signs of right hemisphere lesions were present indicating disturbances of a spatial type. The patient could no longer grasp the concept of numerical value and showed severe difficulties in relation to time. On a linguistic level, the discussion is first considered from a typological point of view; this allows to compare our patient's disorders with a Broca's then with a conduction aphasia, Secondly, the discussion is considered from a semiological point of view, taking into consideration the 10 selected cases in the literature and adding our own; a semiological formula of crossed aphasia is given: agrammatism and/or dyssyntaxia + phonemic paraphasia and/or dysorthographia. A suggestion concerning the role of each hemisphere in the language of our patient is proposed: the possible role played by a congenital deafness in the right ear (discovered in the patient at the age of 8) to explain this abnormal hemispherical functional specialisation is discussed. Original comprehension difficulties concerning the time-space lexic are replaced by a perspective of a cognitive type. We conclude that in our patient, there was a "breakdown" of time and space which comes close to the "indifferenciation" of spatial order and time which Piaget has described in children.

Confusion vs Broca Aphasia: A Case Report.

Broca aphasia presents with impaired expression of spoken and/or written language and is often caused by infarction in the Broca area in the frontal lobe. We present a case of Broca aphasia that was initially interpreted as confusion. A 76-year-old woman was brought to the Emergency Department because of confusion and slurred speech that began in the morning. The patient had an extensive history of alcohol abuse, hyperlipidemia, and hypertension and had recently quit drinking 5 days earlier. The patient appeared confused, answering questions with "I don't know," but had no signs of agitation. Magnetic resonance imaging of the brain confirmed a recent infarct involving the left frontal and occipital lobes, coinciding with the Broca area. The patient was able to communicate via writing and eventually made an uneventful recovery of speech. This case demonstrates a patient without the display of stereotypical signs of stroke, yet that was the underlying condition leading to her aphasia. It is important for clinicians to be aware that a stroke can present with isolated findings such as language deficit or confusion.

[Cerebrovascular disorder and the language areas].

Recent progress of imaging techniques has achieved precise descriptions of aphasic syndromes associated with cerebrovascular disorders. Infarction of the left anterior cerebral artery brings about transcortical motor aphasia. Occlusion of each branches of the left middle cerebral artery produces characteristic language symptoms. Recently, cases with infarction of the areas of prefrontal and precentral arteries were reported to manifest fluent aphasia indistinguishable from the classical transcortical sensory aphasia. Rare cases with lesions restricted to the Broca's area (territory of the precentral artery) produces aphasia with normal fluency, word finding difficulty and deficit in sentence comprehension. Classical non-fluent Broca's aphasia is caused by infarctions which at least involves the areas of precentral and central arteries. Aphemia or pure word dumbness results from damages which involves territory of the central artery. Conduction aphasia is most often associated with lesions of the posterior parietal artery territory. As in the case of Broca's aphasia, Wernicke's aphasia is a composite of conduction aphasia, pure word deafness, transcortical sensory aphasia, and alexia with agraphia. The lesion of Wernicke's aphasia naturally involves the areas of all of these aphasic symptoms. Transcortical sensory aphasia is associated with lesions in the posteroinferior temporal region, and is often associated with watershed infarctions of the middle and posterior cerebral arteries. Aphasia which results from putaminal hemorrhage has ambiguous manifestation, and is difficult to be classified into Wernicke-Lichtheim's model. Assessment of its fluency is notoriously difficult. Thalamic aphasia is similar to either anomic aphasia or transcortical sensory aphasia. It was pointed out that classical aphasic syndromes are still valid as cerebral arterial occlusion syndromes, but are insufficient for the purpose of more precise anatomo-clinical correlation.

[A case of conduction aphasia due to small infarction in the left parietal lobe].

This is a report on the patient with conduction aphAsia due to small infarction in the left parietal lobe. The patient is a right-handed man aged 74, who developed a speech disorder and mild paralysis of the right hand on November 13. 1996. A CT scan showed a small low-density in the supramarginal gyrus of the left parietal lobe. Standard Language Test of aphasia (SLTA) conducted at five days after admission to the hospital showed preserved auditory comprehension and phonemic para-aphasia symptoms with respect to volitional speech, naming, reading aloud and repetition. Frequent self-correction was also observed while repetition was not remarkably impaired. A test at three months after the onset revealed generally fluent speech, while there still remained occasional phonemic para-aphasia and self-correction for the speech disruption. Three years and four months later, most of the aphasic syndromes disappeared, although the patient claimed he still had difficulty in speaking. This case suggests that conduction aphasia can be caused by a lesion, though small, located in arcuate fibers of the cerebrum. The characteristics are phonemic para-aphasia with respect to general speech functions as well as self-correction toward target words. The indicated that lesions in the pathway connecting Broca's area and Wernicke's area causes difficulties in selecting accurate phonemes due to a malfunctioning interface between the two areas.

[Cerebral lateralization in two cases of crossed dextral aphasia with right-hemisphere arteriovenous malformation].

This paper reports two cases of crossed dextral aphasia. The first patient was a 60-year-old right-handed male with no family history of sinistrality. He experienced sudden onset of left hemiplegia and loss of consciousness. A CT scan showed high-density area in the right fronto-parietal region. An angiography revealed an arteriovenous malformation (AVM) in the right parietal lobe. It was fed by a branch of the middle cerebral artery and drained through a cortical vein. Neuropsychological examination one week after the surgery showed severe defects of all language moderalities. He was alert and cooperative, but completely mute. He recognized common words by auditory and visual stimuli, but could not perform simple command. He wrote some meaningless letters when asked to write his own name. Auditory and reading comprehension gradually improved thereafter, but Broca's type of aphasia with non-fluent hesitant and effortful output was still present four months after the surgery. The second patient was a 38-year-old right-handed male. All members of this family are right-handed except for one sister who is left-handed. He suddenly suffered left hemiparesis and loss of consciousness. A CT scan disclosed a right parietal intracerebral hematoma. And an AVM which was fed by the angular artery and drained through a cortical vein was angiographically demonstrated in the same area. Postoperatively the left hemiparesis rapidly disappeared, but left homonymous hemianopsia and anomic type of aphasia still persisted. His speech was fluent and daily communication was possible in spite of circumlocutory paraphasic output.(ABSTRACT TRUNCATED AT 250 WORDS)

[A case of crossed aphasia in a dextral patient with polycythemia].

We report a 72-year-old right-handed man who was diagnosed as having crossed aphasia. He had polycythemia, hypertension and an old cerebral infarction in the right occipital lobe. He was admitted to our hospital because of muscle weakness in the left extremities at the age of 71. In the laboratory data, red blood cells(689 x 10(4)/microliter) and platelets(87.6 x 10(4)/microliter) were increased in number. Brain CT detected a right putaminal hematoma and an old infarct in the occipital lobe on the right. After admission, he developed non-fluent speech, and impairments of auditory comprehension, writing and naming due to the infarction in his right cerebral hemisphere including the middle cerebral artery distribution. The standard language test of aphasia(SLTA) revealed marked impairments in the language function, except for reading kana and kanji words. This writing was severely impaired compared with other language dysfunctions. Auditory comprehension, repetition and reading were impaired at the sentence level rather than at the kana word level. Furthermore, he suffered from left hemiparesis and left unilateral spatial neglect. We diagnosed his impairments of language function as crossed aphasia based on his right-handedness, CT findings and the results of SLTA. His language center was considered to be located in both cerebral hemispheres. Compared with typical findings in reported cases of crossed aphasia, the presence of both non-fluent speech and mutism were consistent with previous observations. However, the marked impairments of auditory comprehension, repetition and naming were different. Polycythemia and hypertension were considered to be the risk factors of cerebral infarction in our patient.

Proper name anomia after right-hemispheric lesion: a case study.

This study describes the case of CH, a 68-year-old left-handed woman who suffered a right temporo-parieto-occipital infarct in the territory of the middle cerebral artery and who exhibits severe proper name anomia. During the acute stage, CH was diagnosed with severe amnestic aphasia (Aachen Aphasia Test). Her lesion mirrors those of left hemisphere impairing the processing proper names, without an aphasic language disorder in general. Seven weeks later, language improved to a mild amnestic aphasia that currently does not interfere with her daily life. However, the use of proper names in both the visual and auditory modalities was still impaired and showed no improvement after 6 months of speech therapy. While not being able to name family members or familiar persons, she was, however, still able to describe the persons' backgrounds along with some additional semantic information. Furthermore, in a simple semantic design test, CH was selectively impaired in correctly classifying proper names into their respective word classes. Conversely, she was able to correctly name and classify other word categories (e.g., common nouns). In the subsequent study, we assessed the modalities "auditory comprehension," "picture naming," and "reading comprehension" and classified her responses in the categories "correctly named," "correctly classified," "correctly described attributes" (e.g., occupation) and "falsely named." The results were compared with those of an age-matched healthy control group. In the visual task, CH correctly named 80% of the visualized objects, 3% of the familiar persons and 15% of the familiar city views.

[Transcortical sensory aphasia due to extensive infarction of left cerebral hemisphere].

We report a case of transcortical sensory aphasia occurred after extensive infarction of left cerebral hemisphere. A 68-year-old, right-handed man with atrial fibrillation suddenly developed cerebral embolism of left middle cerebral artery. He was treated conservatively, and the right hemiplegia, aphasia, apraxia in a slight degree and right hemispatial neglect in a slight degree consequently existed. MRI showed a large cortical and subcortical infarct lesion including the left Broca's area, central region, perisylvian area with Wernicke's area and temporal lobe. In contrast, neuropsychological evaluation using the Western Aphasia Battery (WAB) demonstrated transcortical sensory aphasia, e.g., fluency 8, auditory comprehension 1. repetition 10 and object naming 2.4. In addition to preserved repetition, both linguistic prosody and affective prosody were well preserved. Most cases with transcortical sensory aphasia are known to occur with the lesion including temporo-parieto-occipital junction of dominant hemisphere. Our patient and a few other reported cases of transcortical sensory aphasia had a lesion in perisylvian area including Wernicke's area. Therefore, it is possible that their minor hemisphere worked selectively for repetition. Furthermore, we suggest that this patient presented dissociative aphasia that all the process of repetition and the function of linguistic and emotional prosody were represented in the right hemisphere and the other functions including comprehension of word meanings were existed in the left hemisphere. We believe that our case of transcortical sensory aphasia with dissociative aphasia gives a suggestion about the mechanism and localization of repetition and prosody in the whole system of language.

Subcortical crossed aphasia.

A 55 year-old, right-handed, hypertensive woman with global aphasia, due to a spontaneous hemorrhage in the right putamen extending to the periventricular white matter was examined thirteen days after the acute onset of stroke. She had left hemiplegia and inability to speak. She displayed no spontaneous speech output and was capable only of occasional undifferentiated grunts in conversation. Other language modalities such as auditory and reading comprehension, naming, repetition and writing were severely impaired. Her aphasia was classified as global aphasia. Forty-five days after the onset of stroke, rapid recovery from the aphasia with mild deficits in speaking, naming, and repetition was detected. This case is a good example of crossed aphasia, favouring the importance of deep structures of the right hemisphere in this type of aphasia. Rapid recovery is an important feature.

Thalamic aphasia associated with mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes: A case report.

Mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) with aphasia is a rare disorder, with the associated aphasia reported as either Wernicke's or Broca's. Herein, we report a patient with MELAS complicated by thalamic aphasia. A 15-year-old right-handed girl presented with headache, nausea, right homonymous hemianopsia, and aphasia. She could repeat words said by others, but had word-finding difficulty, paraphasia, and dysgraphia. Brain MRI revealed abnormal signals from the left occipital lobe to the temporal lobe and left thalamus, but Wernicke's area and Broca's area were not involved. Additionally, she had short stature, lactic acidosis, bilateral sensorineural hearing loss, and a maternal family history of diabetes and mild deafness. Based on clinical findings and the presence of a mitochondrial A3243G mutation, she was diagnosed with MELAS. With treatment, the brain MRI lesions disappeared and her symptoms improved. Her aphasia was classified as amnesic aphasia because she could repeat words, despite having word-finding difficulty, paraphasia, and dysgraphia. Based on MRI findings of a left thalamic lesion, we diagnosed her with thalamic aphasia. Thalamic aphasia may be caused by MELAS. Assessment of whether repetition is preserved is important for classifying aphasia.

Mixed transcortical aphasia

In this rare type of aphasia, Broca's area, Wernicke's area, and the arcuate fasciculus are intact but the watershed region around them is damaged. This damage isolates these areas from the rest of the brain. The most frequent etiology of mixed transcortical aphasia is stenosis (narrowing) of the internal carotid artery. Mixed transcortical aphasia can also occur after cerebral hypoxia, cerebral swelling, and any stroke that affects the cerebral artery. Often lesions that cause mixed transcortical aphasia affect both the anterior and posterior perisylvian border zones. Some times the type of aphasia can be determined just by knowing the lesion location. In order for a patient to be diagnosed with mixed transcortical aphasia all other forms of transcortical must be ruled out. Using WAB or the BDAE can rule out global aphasia if the ability to repeat is present. If verbal fluency is depressed transcortical aphasia gets ruled out and if auditory processing and comprehension is weak then

Wernicke's area

Diagnosis of aphasia, as well as characterization of type of aphasia, is done with language testing by the provider. Testing should evaluate fluency of speech, comprehension, repetition, ability to name objects, and writing skills. Fluency is assessed by observing the patient's spontaneous speech. Abnormalities in fluency would include shortened phrases, decreased number of words per minute, increased effort with speech, and agrammatism. Patients with Wernicke's aphasia should have fluent speech, so abnormalities in fluency may indicate a different type of aphasia. Comprehension is assessed by giving the patient commands to follow, beginning with simple commands and progressing to more complex commands. Repetition is evaluated by having the patient repeat phrases, progressing from simple to more complex phrases. Both comprehension and repetition would be abnormal in Wernicke's aphasia. Content should also be assessed, by listening to a patient's spontaneous or instructed speech.

[Spontaneous speech disturbances in so called transcortical motor aphasia--comparison of 3 cases with the different lesion sites].

So called transcortical motor aphasia (TCMA) is frequently subdivided, because the clinical features and the localization of the lesions are variable. The authors have been attempting to classify TCMA into three types according to the distribution of the lesions, such as Type F 1, Type F 2 and Type F 3. Case 1 N.S. belongs to Type F 1 showing the clinical features of TCMA with bleeding in the territory of the left anterior cerebral artery. Case 2 M.E. belongs to Type F 2 (published case). This case is similar to Luria's dynamic aphasia in its clinical features and results from the lesions including the posterior parts of left middle frontal gyrus. Case 3 N.T. belongs to Type F 3 who recovered from typical Broca aphasia after language training for four years. The case is similar to Goldstein's Type 1 of TCMA in its clinical features. These three cases are compared with regard to the fundamental bases of spontaneous speech disturbance. The items of comparison are as follows; the volume of speech production and the the time taken to start speech, word fluency test, cue effects necessary for the success of sentence constructions grammatical ability. The results are summerized in Table 2. Type F1 shows the most conspicuous defect of spontaneous speech, but no disturbance in grammatical ability. And when the top word of a sentence (a subject word) is given by the examiner, the patient can construct a structurally correct sentence. These findings imply that the spontaneous speech disturbance of Type F 1 is due to a defect of the starting mechanism of speech.(ABSTRACT TRUNCATED AT 250 WORDS)

Mixed transcortical aphasia

Symptoms and language characteristics Mixed transcortical aphasia is characterized by severe speaking and comprehension impairment, but with preserved repetition. People who suffer mixed transcortical aphasia struggle greatly to produce propositional language or to understand what is being said to them, yet they can repeat long, complex utterances or finish a song once they hear the first part. Persons with mixed transcortical aphasia are often nonfluent, and in most cases do not speak unless they are spoken to, do not comprehend spoken language, cannot name objects, and cannot read or write. However, they often have the ability to repeat what is said to them. In fact, persons with mixed transcortical aphasia often repeat in a parrot-like fashion. Some patients with this disorder can experience many different types neurological symptoms including, bilateral paralysis, lack of voluntary speech, and difficulty with producing spontaneous speech.

[Transcortical sensory aphasia following a left frontal lesion--case report].

We report a patient with transcortical sensory aphasia (TCSA) following a left frontal lesion. The patient was a 63-year-old right handed Buddhist priest admitted to our hospital with a complaint of word-finding difficulty. Neurological examination failed to reveal any abnormal findings except aphasia. The patients spontaneous speech was fluent, not agrammatic, and free of phonemic paraphasia but he sometimes exhibited semantic paraphasia. His ability to repeat sentences was excellent, but he had severe difficulty in word-finding, auditory comprehension and writing. He read aloud correctly, but his reading comprehension of kana (phonograms) was poor in contrast to excellent reading comprehension of kanji (morphonograms). His clinical picture was characterized by poor comprehension but excellent repetition, and a diagnosis of TCSA was made. CT and MRI revealed an infarction involving the pars opercularis and pars triangularis in the inferior frontal gyrus and the anterior portion of the lower prefrontal gyrus and the middle frontal gyrus. Regional cerebral blood flow was measured by single photon emission CT and was found to be decreased in the same region as indicated on CT and MRI. The clinical picture in this patient was comparable to that of TCSA due to a posterior parieto-occipital lesion, but the rapid improvement (within 1 to 2 months) of this patient was characteristic. Auditory comprehension, kana (phonograms) reading comprehension, and word recall, which were severely impaired in this patient, all demand interaction between phonological processes and semantic processes. Thus we conclude that this patient had impairment of the phonological-semantic interaction process.

Anomic aphasia

Anomic aphasia (also known as dysnomia, nominal aphasia, and amnesic aphasia) is a mild, fluent type of aphasia where individuals have word retrieval failures and cannot express the words they want to say (particularly nouns and verbs). Anomia is a deficit of expressive language. Anomia is a symptom of all forms of aphasia, but patients whose primary deficit is word retrieval are diagnosed with anomic aphasia. Some level of anomia is seen in all of the aphasias. Individuals with aphasia who display anomia can often describe an object in detail and maybe even use hand gestures to demonstrate how the object is used, but cannot find the appropriate word to name the object. Patients with anomic aphasia have relatively preserved speech fluency, repetition, comprehension, and grammatical speech.

Aphasia

Individuals with conduction aphasia have deficits in the connections between the speech-comprehension and speech-production areas. This might be caused by damage to the arcuate fasciculus, the structure that transmits information between Wernicke's area and Broca's area. Similar symptoms, however, can be present after damage to the insula or to the auditory cortex. Auditory comprehension is near normal, and oral expression is fluent with occasional paraphasic errors. Paraphasic errors include phonemic/literal or semantic/verbal. Repetition ability is poor. Conduction and transcortical aphasias are caused by damage to the white matter tracts. These aphasias spare the cortex of the language centers but instead create a disconnection between them. Conduction aphasia is caused by damage to the arcuate fasciculus. The arcuate fasciculus is a white matter tract that connects Broca's and Wernicke's areas. People with conduction aphasia typically have good language comprehension, but poor

Complex partial seizures and aphasia as initial manifestations of non-ketotic hyperglycemia. Case report.

We describe a case of non-ketotic hyperglycemia (NKH), heralded by complex partial seizures and aphasia of epileptic origin, besides versive and partial motor seizures. This clinical picture was accompanied by left fronto-temporal spikes in the EEG. The seizures were controlled by carbamazepine only after the control of the diabetes. A month later, carbamazepine was discontinued. The patient remained without seizures, with normal language, using only glybenclamide. Complex partial seizures, opposed to simple partial seizures, are rarely described in association to NKH. Epileptic activity localized over language regions can manifest as aphasia.

Mixed transcortical aphasia

For most patients, formal and informal language assessments are initially administered during his/her acute hospital stay by a licensed speech-language pathologist. However, a standardized assessment may provide further information regarding an aphasia classification. While there are different classifications of aphasia (i.e., Broca’s, Wernicke’s, Conduction, Anomia), they each have hallmark deficits. Research has shown, a patient presenting with mixed transcortical aphasia will have impairments in all communicative areas, with the exception of the preserved ability to repeat a person’s words or phrases. Patients with mixed transcortical aphasia demonstrate similar deficits as those seen in patients with global aphasia. Therefore, assessment of repetition is most critical in order to differentially diagnose. Specifically, language based standardized assessments such as the Western Aphasia Battery (WAB), and the Folstein Mini Mental State Exam include a repetition subtest amongst

A case of foreign accent syndrome.

Foreign accent syndrome is a rare but potentially devastating clinical condition associated with altered speech rhythm and prosody, often occurring after a cerebral vascular accident. Missing this diagnosis can lead to delayed stroke work-up and treatment. We report a case of foreign accent syndrome in a 60-year-old woman who presented to the Emergency Department (ED) with 3 weeks of altered speech pattern, widened gait, bilateral leg heaviness, and mild headache. The patient had a history of Type 2 diabetes, malignant hypertension, toxic nodular goiter, and hyperlipidemia. She initially presented to the ED at the onset of symptoms, was thought to have had speech change secondary to a goiter impinging on the recurrent laryngeal nerve, and was discharged. She returned to the ED 3 weeks later when outpatient imaging revealed subacute infarction of the left hemi-pons and absent flow within the left vertebral artery. On examination, the patient was alert and conversational. She spoke fluently with an accent that had components of Jamaican and the accent of an Italian speaking English. Neurology was consulted and the patient was admitted. The patient was treated medically, and was discharged home with primary care follow-up. She developed a second, more significant stroke 1 month later, with unilateral weakness and slurred speech in the middle cerebral artery distribution. Clinicians should be aware that some stroke patients present with various atypical symptoms, and should suspect stroke in any patient with acute-onset neurological symptoms, including speech change.

Aphasia

Recent classification schemes adopting this approach, such as the Boston-Neoclassical Model, also group these classical aphasia subtypes into two larger classes: the nonfluent aphasias (which encompasses Broca's aphasia and transcortical motor aphasia) and the fluent aphasias (which encompasses Wernicke's aphasia, conduction aphasia and transcortical sensory aphasia). These schemes also identify several further aphasia subtypes, including: anomic aphasia, which is characterized by a selective difficulty finding the names for things; and global aphasia, where both expression and comprehension of speech are severely compromised. Many localizationist approaches also recognize the existence of additional, more "pure" forms of language disorder that may affect only a single language skill. For example, in pure alexia, a person may be able to write but not read, and in pure word deafness, they may be able to produce speech and to read, but not understand speech when it is spoken to them.

Type of aphasia: relationship to age, sex, previous risk factors, and outcome of rehabilitation.

Relationship of types of aphasia in hemiplegics to survival, outcome of rehabilitation, activities of daily living (ADL) and pre-existing risk factors, hypertension (HT), ischemic heart disease (IHD), diabetes mellitus (DM) were studied in a group of 257 patients. The control group was a large population of CVA cases previously documented. Four main categories were considered: expressive-receptive (global), predominantly expressive (Broca), predominantly receptive (Wernicke) and predominantly amnestic (anomia) aphasias. 40% of each category were female. No clear pattern emerged concerning relationship with risk factors; however, hypertension, the factor most frequently encountered, was significantly less prevalent among expressive ahphasics, and diabetes mellitus was rare among those with the receptive pattern. For all categories, the most frequent etiology was thrombosis, the second being embolia. The oldest groups were the expressive-receptive and the predominantly receptive aphasia groups: showed the poorest rehabilitation outcome in both ADL and locomotion, and lived less time after stroke (5.8 years). Amnestic and expressive patients were younger and fared better in all other parameters; an etiology of embolia was much more frequent among the former. It can be said that patients with the expressive-receptive kind of aphasia have the worst survival and rehabilitation prognoses.

Conduction aphasia

History In the late 19th century, Paul Broca studied person with expressive aphasia. These person had lesions in the anterior perisylvian region (now known as Broca's area), and produced halting and labored speech, lacking in function words and grammar. For example: Comprehension is generally preserved, although there can be deficits in interpretation of complex sentences. In an extreme example, one of his person could only produce a single syllable, "Tan". Meanwhile, Carl Wernicke described person with receptive aphasia, who had damage to the left posterior superior temporal lobe, which he named "the area of word images". These person could speak fluently, but their speech lacked meaning. They had a severe deficit in auditory comprehension. For example, "Clinician: What brings you to the hospital? The two disorders (expressive and receptive aphasias) thus seemed complementary, and corresponded to two distinct anatomical locations.

Transcortical sensory aphasia

Transcortical sensory aphasia (TSA) is a kind of aphasia that involves damage to specific areas of the temporal lobe of the brain, resulting in symptoms such as poor auditory comprehension, relatively intact repetition, and fluent speech with semantic paraphasias present. TSA is a fluent aphasia similar to Wernicke's aphasia (receptive aphasia), with the exception of a strong ability to repeat words and phrases. The person may repeat questions rather than answer them ("echolalia").

[A case of pure word deafness and auditory agnosia associated with bilateral temporo-parietal lesions].

A-49-year-old right-handed female was reported. She showed pure word deafness and auditory agnosia because of bilateral temporo-parietal lesions. The left lesion resulted from angiospasm of the left anterior and middle cerebral arteries after subarachnoid hemorrhage due to a ruptured aneurysm of the left carotid artery, and the right one resulted from subcortical hematoma after the V-P shunt operation. CT scan revealed the abnormal low density area on the bilateral temporo-parietal regions seven months after onset. Neurophychological findings were as follows: there were no aphasic symptoms such as paraphasia, word finding difficulties, or disturbances of spontaneous writing, reading and calculation. But her auditory comprehension was severely disturbed, and she could neither repeat words after the tester nor write from dictation. She also could not recognize meaningful sounds and music in spite of normal hearing sensitivity for pure tone, BSR and AER. We discussed the neuropsychological mechanisms of auditory recognition, and assumed that each hemisphere might process both verbal and non-verbal auditory stimuli in the secondary auditory area. The auditory input may be recognized at the left association area, the final level of this mechanism. Pure word deafness and auditory agnosia of this case might be caused by the disruption of the right secondary auditory area, the pathway between the left primary auditory area and the left secondary auditory area, and between the left and right secondary auditory areas.

Transcortical sensory aphasia due to a left frontal subcortical haemorrhage.

A case of transcortical sensory aphasia caused by a cerebral haemorrhage in the left frontal lobe is presented. A 72-year-old right-handed woman was admitted to the hospital, with a history of acute onset of speech disturbance and headache. On initial assessment, her spontaneous speech was fluent. She had no difficulty initiating speech, articulated normally, and did not exhibit logorrhea. Her ability to repeat phonemes and short sentences (5-6 words) was fully preserved, however she had severe difficulty with visual recognition of words, and with aural comprehension at the word level, although she was able to read words aloud. Computed tomography and magnetic resonance imaging showed cerebral haemorrhage in the left frontal lobe, involving the superior and middle frontal gyrus. Single photon emission CT revealed a wider area of low perfusion over the entire left frontal lobe, including the superior, middle and inferior frontal gyrus. The aphasia symptoms, mainly poor comprehension, disappeared quickly several weeks after the event. This may have been due to a reduction in the size of the haematoma and a resolution of the oedema around the haematoma. Clinically, the transcortical sensory aphasia in this case was indistinguishable from that caused by damage to the posterior language areas. Further case reports of transcortical sensory aphasia associated with frontal lobe lesions would help to confirm whether a relatively rapid recovery is characteristic in cases such as this.

[50-year-old patient with dyspnea, dizziness, palpitations and brief sensory aphasia].

After a syncope, a 50 years old female patient was administered with an incomplete central facial paralysis on the left side combined with dyspnea, tachycardia, and hypotension as well as a systolic nurmur over the tricuspid valve. One week before, a vein stripping of the left long saphenous vein had been undertaken. By doppler-ultrasound, a thrombosis of the left tibial veins could be found as the cause of the pulmonary embolism. Additionally, the echocardiogram showed a relative tricuspid insufficiency and a floating atrial septum combined with an enlarged right atrium as an expression of the pulmonary hypertension. The incomplete central facial paralysis must be due to a paradox embolism in the cerebrovascular circulation as a result of an open foramen ovale. Under a therapy with high-dose heparin, all findings receded totally within one week.

[Postictal aphasia and its generating mechanism in 3 patients with localization-related epilepsy].

Semiology of postictal aphasia as well as its generating mechanism involving both the epileptogenic zone and language area has not yet been sufficiently elucidated. Therefore, postictal aphasias were studied in 3 patients with localization-related epilepsy. Postictal motor aphasia was observed in a patient (patient 1) with frontal lobe epilepsy whose recovery of language function progressed from loss of language function, to Broca's aphasia, and eventually to poor spontaneous speech. Postictal sensory aphasia was observed in 2 patients (patient 2 and 3) with temporal lobe epilepsy whose recovery of language function progressed from loss of language function, to jargon, and eventually to circumlocutory anomic speech. Both patient 2 and 3 did not show fluent speech. Seizure manifestations, EEG, IMP-SPECT and MRI indicated that epileptogenic zones were in the left frontal lobe including Broca's area in patient 1, the mesial part of the left temporal lobe in patient 2, and the middle and posterior part of the left temporal lobe including Wernicke's area in patient 3. A postictal verbal dichotic listening test showed the reduction of correct responses by right ear in the patient 3. Postictal auditory verbal learning tests showed the impairment of verbal memorization in patient 2 and 3. The impairment of verbal memorization was particularly marked in patient 2. These results suggest that 1) the characteristics of postictal motor and sensory aphasia are clearly elucidated by analyzing the sequence of recovery from postictal language dysfunction, 2) postictal aphasia is generated by the epileptogenic zone involving the language area or the ictal discharges propagating to the language area, and 3) not only the disturbance of language function, but also the impairment of verbal memorization seems to participate in the disturbance of repeating and understanding sentences in the patient with postictal sensory aphasia.

[Slowly progressive fluent aphasia--clinical features and an imaging study including MRI, SPECT and PET].

Three cases of slowly progressive fluent aphasia were presented. In all it began with word amnesia or stuttering, and in one to five years impairment of auditory comprehension, and reading and writing difficulties with kanji (Japanese morphograms) appeared. The neuropsychological and radiological findings were as follows: Case 1: a right-handed 65-year-old man showed severe fluent aphasia (the Western Aphasia Battery profile was rated as corresponding to Wernicke's aphasia but his score on the Token test was too high for Wernicke's aphasia) and memory disturbance. Cortical atrophy was prominent in the left temporal and parietal lobes. Hypoperfusion was evident in the bilateral anterior temporal region, suggesting the diagnosis of Pick's disease. Case 2: a right-handed 42-year-old man presented amnesic aphasia with buccofacial and ideomotor apraxia. The left frontal, temporal and parietal lobes were all atrophic. Hypoperfusion was marked in the left perisylvian and temporo-parietal regions, being similar to the pattern of Mesulam's slowly progressive aphasia. Case 3: a right-handed 55-year-old man with amnesic aphasia. Left-side dominant cortical atrophy involved the frontal, temporal and parietal lobes. The metabolic rate was lower in the left anterior temporal lobe, compatible with the finding in Pick's disease. The common clinical features of these patients were selective deficits in vocabulary, resulting in impairment of confrontation naming, and auditory comprehension. They sometimes could not recognize things even when they were told their names; case 1 could not even point to objects on command, while their syntactic comprehension was well preserved.(ABSTRACT TRUNCATED AT 250 WORDS)

Anomic aphasia

Although not many literary cases mention anomic aphasia, many nonfiction books have been written about living with aphasia. One of them is The Man Who Lost His Language by Sheila Hale. It is the story of Hale's husband, John Hale, a scholar who suffered a stroke and lost speech formation abilities. In her book, Hale also explains the symptoms and mechanics behind aphasia and speech formation. She adds the emotional components of dealing with a person with aphasia and how to be patient with the speech and communication. See also Conduction aphasia Expressive aphasia Lists of language disorders Primary progressive aphasia Receptive aphasia Tip of the tongue References External links Aphasias Dementia Stroke Speech and language pathology Language disorders Communication disorders de:Aphasie#Amnestische bzw. anomische Aphasie id:Disnomia pl:Dysnomia (choroba) sv:Dysnomi

Transcortical sensory aphasia

Transcortical sensory aphasia is characterized as a fluent aphasia. Fluency is determined by direct qualitative observation of the patient’s speech to determine the length of spoken phrases, and is usually characterized by a normal or rapid rate; normal phrase length, rhythm, melody, and articulatory agility; and normal or paragrammatic speech. Transcortical sensory aphasia is a disorder in which there is a discrepancy between phonological processing, which remains intact, and lexical-semantic processing, which is impaired. Therefore, patients can repeat complicated phrases, however they lack comprehension and propositional speech. This disconnect occurs since Wernicke’s area is not damaged in patients with TSA, therefore repetition is spared while comprehension is affected. Patients with intact repetition can repeat both simple and complex phrases spoken by others, e.g. when asked if the patient would like to go for a walk, he or she would respond "go for walk." Although patients can

Subcortical anarthria: a case report.

A 56-year-old right-handed male with a history of hypertension and diabetes presented two episodes of stroke: The first affected territory was the left anterior coroidal artery (capsular and paracapsular infarcts at the level of the genu and posterior arm of the internal capsule) and the second was the right thalamus, due to a hematoma. Following the first stroke, the patient developed severe dysarthria and after the second stroke remained anarthric. The pathophysiology of the disorder is discussed, and the role of the left and right thalamus as far as speech is concerned is reviewed.