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PubMed1990

[Familial idiopathic vitamin E deficiency associated with cerebellar atrophy].

Sibling cases of familial vitamin E deficiency accompanied by ataxia, polyneuropathy and mental retardation were reported. Case 1 was a 37-year-old male who developed progressive gait disturbance, deformity of the feet and head tremor from childhood, after normal delivery and development of early childhood. On physical examination, he had cataract, high arched palate and pes cavus. Neurological examination revealed mental retardation (WAIS 68), scanning speech, muscular atrophy of the face and extremities with predominance in the lower limbs, absent Achilles tendon reflex, disturbance of superficial and deep sensation predominant in distal limbs, and marked gait ataxia. Ataxia was both cerebellar and sensory in nature. Laboratory data of the blood showed no significant abnormalities including blood glucose and vitamin B12 except a markedly low level of serum vitamin E. The brain CT scan revealed severe cerebellar atrophy and marked dilatation of the cisterna magna and the subarachnoid space around the cerebellum. Motor nerve conduction velocity in the leg was decreased. Biopsy specimen from the quadriceps muscle showed neurogenic atrophy. Sural nerve biopsy revealed decrease in large myelinated fibers with axonal degeneration and regeneration. Oral administration of alpha-tocopherol acetate, 600 mg per day, diminished ataxia significantly. Based on lysosomal enzyme activity in leukocytes, clinical and laboratory examination, lipidosis or spinocerebellar degeneration was excluded. Chronic lipid malabsorption or beta lipoprotein deficiency which can cause decrease in vitamin E absorption, was not recognized. On oral loading with 2 g of alpha-tocopherol acetate, the decrease rate of serum vitamin E was normal. Consequently the low vitamin E was considered to have resulted from selective impairment of vitamin E absorption.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Charcot-Marie-Tooth disease: a case presenting with hyperreflexia.

We report a 10-year-old girl with progressive weakness of lower extremities, feet deformity, and sensory impairment on both feet for 3 years. Absent ankle tendon reflex, exaggerated knee jerk and prolonged nerve conduction velocity were noted by physical and electrophysiological examination. Nerve and muscle biopsy showed demyelination and neurogenic changes respectively and supported the diagnosis of Charcot-Marie-Tooth disease, type I. The point that the diagnosis of Charcot-Marie-Tooth disease remains possible even in the absence of family history and the typical clinical picture is stressed. Complete electrophysiological study and tissue diagnosis are required for early diagnosis, early rehabilitation and reconstructive surgery.

Charcot-Marie-Tooth Disease↗
PubMed1990

[Pindolol-induced rhabdomyolysis in sarcoid myopathy].

A 72-year-old man suddenly developed severe muscle weakness following the treatment with pindolol (Calvisken) for three days. Neurological examination on admission disclosed marked proximal muscle weakness with absent deep tendon reflexes. Laboratory data showed significant increase of serum CK, aldolase and myoglobin. Electromyography revealed both neurogenic and myogenic changes in all muscle tested. Skeletal muscle CT showed patchy low density areas in muscles of thigh and leg, especially in the hamstrings. Femoral muscle biopsy demonstrated a granulomatous nodule with multinucleated giant cells in the degenerated muscle fibers showing small-grouped atrophy. By Mb-PAP staining, Mb-negative fibers were randomly distributed among normally stained ones. Leu 1, 3a, 4, HLA-DR positive cells were found adjacent to the granuloma by immunoperoxidase staining. After immediate withdrawal of pindolol and treatment with steroid, he recovered muscle strength and enzyme activities were normalized in a week. Beta blockers have been known to induce muscle cramps or pain and moderate elevation of serum muscle enzymes. However, severe muscle weakness with highly elevated enzyme activities leading to rhabdomyolysis as noticed in the present case was rarely reported in the literature. Underlying sarcoid myopathy might be suspected to exaggerate this unusual case of pindolol-induced rhabdomyolysis. A careful use of pindolol is emphasized.

Aged↗
PubMed1990

[A case of polymyositis associated with primary biliary cirrhosis].

We studied a 67-year-old female suffered from polymyositis associated with primary biliary cirrhosis. She was pointed out liver dysfunction by screening test. Alkaline phosphatase, transaminase, and IgM were increased. Antimitochondrial antibody and antinuclear antibody were positive. Liver biopsy showed cell infiltrations in Glisson's capsules and destruction of cholangioles, being diagnosed as primary biliary cirrhosis (Scheuer Stage I). Four years later she showed a muscle weakness of four extremities and admitted to our department. Neurological examination revealed a severe weakness and atrophy of both proximal and distal muscles. Deep tendon reflex was decreased on four extremities. Laboratory examination showed a creatine kinase level of 312 IU/L, alkaline phosphatase 238 IU/L, gamma-glutamyl-transpeptidase 140 IU/L, Igm 416 mg/dl, antimitochondrial antibody titer 1:320, and antinuclear antibody titer 1:320. Muscle biopsy findings were compatible with polymyositis. Electron microscopic examination disclosed diffuse increase of mitochondria in subsarcolemma and intermyofibrils. Until now eight cases with polymyositis associated with primary biliary cirrhosis have been reported, but electron microscopic examination of muscle has not been carried out. It is necessary to examine mitochondria of muscle and liver in patients with polymyositis associated with primary biliary cirrhosis for the elucidation of its etiology.

Aged↗
PubMed1990

[Clinical and neuroradiological features of syringomyelia associated with Chiari malformation].

The clinical presentation and radiological features were analyzed in 30 cases of syringomyelia associated with Chiari malformation. None of the patients had spinal dysraphism. The age on admission ranged from 6 to 59 years with a mean of 27 years. Syringomyelia was diagnosed by CT myelography and or MRI from 1982 to 1988. The initial symptoms were skeletal abnormality (43%) such as scoliosis (12 cases) or pes cavus (one case), unilateral pain or numbness (40%) and unilateral motor weakness (17%). Frequently seen signs on admission were sensory deficit (100%), scoliosis (57%), muscle weakness (57%), muscle atrophy (37%) and lower cranial nerve palsy (40%). The neurological findings were asymmetrical in all patients. The characteristic neurological findings in the cases presenting under 20 years of age were unilateral sensory and motor deficits (61%) with decreased or absent deep tendon reflex on the same side. The localization of the syrinx in axial section varied according to the level even in the same case. In 15 cases with unilateral sensory disturbance or unilateral sensory and motor deficit, the syrinx was located in the region corresponding to the posterolateral portion on the same side as that of sensory disturbance in the cervical or thoracic level. On the other hand, in 15 cases with bilateral sensory and motor deficit, the syrinx was located in the central portion and extended into the posterolateral portion of the more affected side.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1990

[A case of juvenile Sandhoff disease].

A Japanese male with juvenile Sandhoff disease is described. The patient was a product of full-term normal pregnancy from non-consanguineous parents. Since age 10, he developed progressive dysarthria and proximal muscle atrophy and weakness. Mental deterioration and cerebellar ataxia are also noted since the age of 20. On neurological examination at age 35, he showed decreased mentality (IQ 62), marked atrophy and weakness of proximal muscles, cerebellar ataxia and increased deep tendon reflexes. Brain CT scans revealed moderate to marked atrophy of cerebellum. Giant MUP, fasciculation potentials and positive sharp waves were observed on EMG examination. Biopsied sural nerve showed markedly decreased myelinated fibers. Hexosaminidase A and B activities in leukocytes and cultured fibroblasts were about 10% of normal values, while other lysosomal enzyme activities were within normal range. Rectal biopsy demonstrated lamellar inclusion bodies in submucosal ganglion cells. This is the first Japanese patient with juvenile Sandhoff disease presenting symptoms similar to motor neuron disease and cerebellar degeneration.

Adult↗
PubMed1990

[Encephalomyelitis with elevated serum antibody against Borrelia burgdorferi].

A 60-year-old female was admitted because of intermittent fever, arthralgia, itching of whole body, pretibial edema, urinary incontinence, pain of both legs and gait disturbance, after an insect bite. On admission, she had fever of 38 degrees C, and nuchal pain and stiffness. Neurological examination revealed spasticity of lower legs and increased deep tendon reflexes of all extremities. Hyperesthesia and hyperalgesia were noted on C2-4 and L5-S5 areas. Leukocyte count was 10,100/mm3 and CRP was 2+. CSF showed no pleocytosis (3/mm3, lymphocyte), but total protein (50 mg/dl) and IgG (10.5 mg/dl) were increased. On T2-weighted images of brain MRI, multiple small high signal areas were shown. The symptom improved markedly by prednisolone, but 3 months later left lateral gaze palsy appeared abruptly. A demyelinating lesion of the pons to the medulla oblongata including the left paramedian pontine reticular formation was suspected, and a corticosteroid pulse therapy was very effective. Serum titer of anti-Borrelia burgdorferi-IgG antibody by indirect immunoperoxidase method was 400 x at first and 1600 x after 3 months. Neuroborreliosis was diagnosed, but high doses of intravenous penicillin were not effective, and an immune-mediated demyelinating mechanism was probably thought to play a role in the pathogenesis of neuroborreliosis.

Antibodies, Bacterial↗
PubMed1990

[Oculocerebrorenal sydrome of Lowe. Apropos of three cases].

We report clinical features and course of Lowe's syndrome with regard to three cases. All of them are males and clear inherited transmission was demonstrated in patients 2 and 3 and was suggested in patient 1. Age at the moment of diagnosis oscillated between 7 and 18 years. The three cases showed weight and height percentiles under p 3. Congenital bilateral cataract and search nystagmus were found in all of them. Profound mental retardation, muscular hypotonicity and diminished or absent tendon reflexes constituted distinctive findings in the neurological area. Among renal manifestations stood out proteinuria, generalized hyperaminoaciduria and tubular renal acidosis, they carried from rickets and growth failure. Cases 1 and 2 has characteristic facies. Patient 1 died after series of recurrent bronchial and pulmonary infections: death happened during Fanconi's syndrome evolution. Cases 2 and 3 are in a stabilized period, with a longer life expectation, although they suffer from residual moderate renal failure.

Adolescent↗
PubMed1990

[A case of myotonic dystrophy associated with intracardiac conduction abnormalities and aortic regurgitation].

A rare case of myotonic dystrophy with mechanical derangement in a 48-year-old male is reported. The patient was admitted to Fuzisawa City Hospital because of chest discomfort. On physical examination, he had the typical facial appearance of myotonic dystrophy, and displayed grip myotonia. The blood pressure was 120/60 mmHg and the pulse 51, regular. A systolic ejection murmur at the cardiac base, an early diastolic blowing murmur along the left sternal border, and a pansystolic murmur at the apex were heard. The deep tendon reflexes were all normal. Elevation of serum creatine kinase and aldolase were noted. Chest X-ray films suggested moderate cardiomegaly. An electrocardiogram showed sinus bradycardia, atrioventricular block and left bundle branch block, suggesting diffuse involvement of the conduction system. An echocardiography confirmed the presence of left ventricular enlargement, thickened aortic valves, mitral regurgitation, and aortic regurgitation. Selective coronary angiography revealed no abnormalities. Left ventriculography demonstrated diffuse hypokinesis of the entire ventricle. Light microscopy of biopsied right myocardium revealed prominent interstitial fatty infiltration, mild interstitial fibrosis, and variation in the nuclear size. A 22-year-old son also had myotonic dystrophy and had an echocardiography indicative of thickened valves with aortic regurgitation. Myotonic dystrophy is a autosomal dominant disease. Cardiac involvement selectively disturbs the conduction system, sinus node, and to a lesser extent myocardium. Although the presence of aortic regurgitation could be a mere coincidence, we believe that this did not occur by accident, because the patient's son also had aortic regurgitation.

Echocardiography↗
PubMed1990

[Juvenile Crow-Fukase syndrome with response to bolus of methylprednisolone after failure of treatment by plasma exchange].

A 20-year-old woman was hospitalized because of abdominal distention. She had developed facial edema about one year earlier, and recently amenorrhea and red verrucae on the chest and abdomen. Neurological examination disclosed hypesthesia, paresthesia, and diminished tendon reflexes in the arms and legs. The level of serum immunoglobulin A (IgA) was elevated and an M protein was detected. Examination of the bone marrow disclosed abnormal increase in plasma cells. Results of glucose tolerance test were mildly abnormal. The patient was diagnosed as Crow-Fukase syndrome. Plasma exchange was done four times and melphalan was given orally for two weeks, but the level of serum IgA increased further. Then one bolus injection of methylprednisolone decreased the serum IgA with improvement in other signs. The disorder is now controlled satisfactory with a low dose of prednisolone.

Adult↗
PubMed1990

[MRI findings in a patient with multiple sclerosis and "hyperkinésies voltionnelles" as a main symptom].

A 23-year-old female was admitted to our hospital complaining of tremor in the upper extremities and gait disturbance. Beginning at age 18, this patient experienced tingling of the right fingers, gait disturbance, dysesthesia of both hands, and tremor in the upper extremities. These symptoms disappeared several weeks after each onset. At age 21, gait disturbance and coarse tremor in the upper extremities developed. They were exaggerated and occurred repeatedly. On neurological examination, the right optic disc was slightly pale. She had nystagmus in all directions with ocular movements. Deep tendon reflexes were hypoactive throughout. There was no tremor in the upper extremities at rest, but during the voluntary movements especially in maintaining certain posture coarse tremor developed. When performing goal-directed motion, such as finger-nose test, the tremor became worse near the terminal position. The patient's gait was broad-based, with the trunk trembling. There were no sensory disturbances, dysarthria, or bowel or bladder dysfunction. Laboratory studies were normal except for high IgG% in the cerebrospinal fluid. An electromyogram using surface electrodes recorded rhythmic bursts of about 4c/s, alternating between the extensor and the flexor muscles of the right arm. MRI of T2-weighted images showed many high-intensity areas located around the bilateral ventricles and near the area of the decussation of superior cerebellar peduncle. A diagnosis of multiple sclerosis was made in this case based on the patient's history of illness and MRI findings. The tremor in her right upper extremity was too intense and coarse to be described as tremor, and should better be called "hyperkinésies volitionnelles (HV)".(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

[A case of hereditary motor and sensory neuropathy of neuronal type with retardation of motor development].

An atypical case of hereditary motor and sensory neuropathy of neuronal type with retardation of motor development was described. The patient was a 15-year-old boy who had suffered from distal muscle weakness with atrophy of four limbs and deformities of hands and feet since age 6 months. These symptoms were slowly progressive. He had never walked. His parents were not consanguinous. His parents and two siblings were unremarkable on neurological examination and on nerve conduction studies. On neurological examination, he showed severe degree of muscle weakness and atrophy in the distal upper and lower limbs, moderate degree of muscle weakness and atrophy in the proximal upper limbs and slight degree of made weakness and atrophy in the proximal upper limbs. Deep tendon reflexes in four limbs were decreased or absent. Vibration sensation was moderately decreased in the distal parts of four limbs. On the nerve conduction studies, no sensory nerve potential was recorded in the median, ulnar and sural nerves bilaterally. Motor nerve conduction velocity of the right tibial nerve was 21 m/sec and the amplitude of the compound muscle action potential (M-wave) was 0.15 mV, and no M-wave was elicited with the electrical stimulation of the median, ulnar and peroneal nerves. Neelde EMG showed fibrillation potentials and giant spikes with a reduction of the number of motor units. On sural nerve biopsy, the densities of both myelinated and unmyelinated fibers were severely decreased.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1990

[The effect of euphylline on energy expenditure in obese patients during treatment with a reducing diet].

The energy economy induced by a reducing diet and manifested by a reduced energy output at rest threatens greatly the long-term success of reducing regimes. The authors investigated the effect of a four-week therapy of obese patients by a low energy protein diet with an energy value of 1560 kJ on the resting metabolic rate (RMR), the serum concentration of thyroid hormones and TSH and on the Achilles tendon reflex time. Four weeks' treatment with a low energy protein diet caused a significant drop of the energy output at rest in the control group of obese men (by 17.5%), as well as in the control group of obese women (by 16.9 per cent). In the group of obese women who were given during the last two weeks of treatment depot methyl xanthine derivative, Euphilline (Byk Gulden), the energy output at rest did not decline as a result of dietetic treatment and the decline of the BMI was significantly higher than in the control group of obese women, although the two groups did not differ in the initial BMI, mean age and the degree of physical activity during treatment. With the exception of the control group of men where the serum triiodothyronine level declined, in the investigated obese subjects no significant changes of the investigated thyroid function parameters were recorded. The syndrome of low T3 thus does not participate in a substantial way in the drop of the metabolism at rest during treatment with a low energy protein diet, obviously due to the intake of 50 g carbohydrate per day.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

[Late-infantile form galactosialidosis with psychomotor retardation and spastic paraparesis].

We described a case of late-infantile form of galactosialidosis. This male patient was a product of normal pregnancy. His parents were first cousins. He first sat at eight months, walked and talked at two years of age. His gait gradually became unsteady and he was diagnosed as spastic paraparesis at the age of five years. Abnormally slow learning was first pointed out at seven years of age. At the age of nine years, we evaluated him in detail at our university hospital. Physical examination revealed a short stature for his age, slightly coarse face, short neck, funnel chest, genu, pes and hallucis valgus. Corneal clouding, hernia and angiokeratoma were not found. Neurological examination showed mental retardation, bilateral optic atrophy without cherry-red spots, and spastic and slightly ataxic gait. Slight muscular atrophy with weakness was also seen in the extremities, more remarkable in the lower limbs. Deep tendon reflexes were hyperactive with bilateral ankle clonus and no extensor planter response. Routine examination of blood, urine and cerebrospinal fluid were normal except for approximately 10% lymphocytes containing cytoplasmic vacuoles. X-ray films of the backbone exhibited vertebral plana with anterior breaking at the second lumbar vertebra level. The electroencephalography showed the multiple spike and slow wave complexes. Brain CT depicted the atrophy of cerebellum. The activities of sialidase and beta-galactosidase were markedly reduced in white blood cells and cultured skin fibroblasts in this patient. His urinary excretion of sialyloligosaccharides increased.(ABSTRACT TRUNCATED AT 250 WORDS)

Carbohydrate Metabolism, Inborn Errors↗
PubMed1989

[Paralytic ileus and atonic bladder in a case of mitochondrial encephalomyopathy--electrophysiological, chemical and pathological study with evidence of the peripheral nerve involvement].

A 41-year-old female of mitochondrial myopathy characterized by recurrent paralytic ileus and atonic bladder with the evidence of peripheral nerve involvement was described. This patient was admitted to our hospital because of the episode of paralytic ileus and atonic bladder at the age of 40 and 41 (1987). She had noticed sporadic headache from 1967, constipation from 1977, tinnitus and hearing disturbance from 1984. One month after her second admission in 1987, her symptoms of paralytic ileus and atonic bladder gradually disappeared. She was then transferred to the department of neurology for the evaluation of underlining neurological disorders. Neurological examination revealed dementia, oro-lingual dyskinesia, and proximal muscular weakness. However, none of the following signs or symptoms were observed; Ophthalmoplegia, blepharoptosis, retinitis pigmentosa, myoclonus, cerebellar ataxia, sensory disturbance, and orthostatic hypotension. Deep tendon reflexes were normal. Planter responses were flexor. Pyruvate and lactate were elevated in both serum and cerebrospinal fluid. Brain CT scan displayed moderate cerebral atrophy and basal ganglia calcifications. EMG was normal except for the external anal sphincter muscles which showed a denervation pattern. Motor nerve conduction velocity was normal in the right median and the right peroneal nerves. Sensory nerve conduction velocity was also normal in the right median and the right sural nerves. However, the amplitude of sensory potential was low in both these nerves. Atonic type of neurogenic bladder was noted on cystometry. There was a lack of voiding desire. The number of active sweat glands iontophoretically stimulated by pilocarpine was reduced. The most prominent feature of the muscle biopsy (the left biceps brachii) was myopathic changes with ragged-red fibers.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

[Subacute myeloneuropathy after abuse of nitrous oxide: an electron microscopic study on the peripheral nerve].

We have experienced a case of myeloneuropathy following habitual abuse of nitrous oxide. We report clinical and pathological findings of this case with review of literatures. A 36-year-old dentist was first admitted to our hospital on August 17, 1983 because of numbness of both lower legs and unsteady gait. He had recreationally inhaled nitrous oxide 30 to 60 minutes everyday since a year ago. Neurological examination showed ataxic broad-based gait, moderate loss of pain and touch sensation in the lower limbs up to patella. Position and vibratory senses were more severely impaired. Deep tendon reflexes increased in the upper extremities and at the knees, but diminished at ankle jerks. Muscle strength was normal. Prominent Lhermitte's sign was present. Except for reduced serum vitamin B12 level, laboratory results were normal. Needle electromyography showed high amplitude and long duration NMU in the right quadriceps and anterior tibial muscles. Motor nerve conduction velocity was 34 m/sec at the right posterior tibial nerve and could not be detected at the left. Sural nerve biopsy was performed. The density of the myelinated fibre measured on transverse section was in normal range but degenerated fibres were occasionally recognized. Single teased nerve fibre showed various degree of myelin ovoid along the fibre. Myelin loss was shown to occur in some parts of the fibre. Electron microscopy showed myelin splitting and formation of intramyelinic vacuoles containing myelin debris. Axon was almost normal at least in the early stage of degeneration. Later, axon disappeared with destruction of myelin sheath. These nerve changes largely demonstrated demyelination but it was occasionally accompanied with axonal degeneration.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

[Acute autonomic and sensory neuropathy associated with galactorrhea-amenorrhea syndrome and intractable anorexia].

Acute autonomic and sensory neuropathy (AASN), one subtype of acute pandysautonomia, in which dorsal root ganglia and autonomic ganglia are involved is uncommon. Little is so far known on central nervous system involvement in AASN. In the present paper we described a rare case of AASN associated with the central nervous system manifestations such as galactorrhea-amenorrhea syndrome and intractable anorexia. A 30-year-old woman rapidly developed burning pain and numbness in her arms and legs as well as orthostatic syncope. She had severe anorexia and no no menstruation from onset. On physical examination, she was emaciated. There was marked orthostatic hypotension with tachycardia. Skin was dry. Moderate galactorrhea was detected. Neurological examination showed prominent paresthesia and dullness of superficial sensation, predominantly to pinprick and thermal stimuli, segmentally over the neck, occipital scalp, and extremities. Deep sensation was intact. She had no weakness or ataxia. Deep tendon reflexes were almost normal. NCV and SEP were normal, while EEG was abnormal. Sural nerve biopsy demonstrated axonal degeneration with the loss of myelinated, predominantly in small-caliber fibers, and unmyelinated fibers. The levels of HVA and MHPG in CSF were decreased. The autonomic nervous function tests revealed postganglionic dysfunction. alpha-adrenergic system was predominantly impaired, while beta-adrenergic system was relatively preserved. The endocrinological studies demonstrated mild or moderate elevation of PRL basal value and hyper-response of PRL and LH for TRH and LH-RH loading test, which suggested disorder of the hypothalamo-hypophysial system. Cranial MRI showed moderate dilatation of the 3rd ventricle.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1989

[Subacute sensory neuropathy manifestated by tonic pupils associated with small cell carcinoma of the lung].

Only a few cases of carcinomatous neuropathy with tonic pupils have been reported. In the present paper we described a 53-year-old woman with subacute sensory neuropathy who had presented with bilateral tonic pupils. She noticed numbness over the medial aspect of the left thigh in March, 1988, and then developed dysesthesia over the left forearm and hand, mild weakness of left upper and lower extremities and urinary disturbance. Neurological symptoms were subacutely progressive and she was bed-ridden in May. She was admitted to our hospital in June, 1988. On examination, she had body-weight loss of 6 kg during the last six months and general status was otherwise unremarkable. She had anisocoria; the left pupil was larger in daylight than the right, while smaller in dim light. The left pupil scarcely reacted to light, but promptly constricted to near vision. The right pupil constricted normally to light and near vision. An instillation of 0.0625% pilocarpine solution showed supersensitive response of both pupils. An instillation of 1.25% epinephrine solution demonstrated mild dilation of both pupils. Thus, it was conceivable that she had postganglionic ciliary nerve damage characteristic of tonic pupil as well as the lesion of sympathetic nerve innervating pupillary dilator. She had severe sensory ataxia and pseudoathetosis of the hands. Weakness was mild to moderate in extremities. Almost all deep tendon reflexes were absent. All modalities of sensation, particularly on deep sense, were severely involved with sea-level-type distribution below Th7, and over C2 to C3 regions on the left side.(ABSTRACT TRUNCATED AT 250 WORDS)

Autonomic Nervous System Diseases↗