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PubMed1988

[Lipid chemical study of an autopsy case of Nasu-Hakola disease].

Lipid chemical analysis of a case of membranous lipodystrophy (Nasu-Hakola disease) was reported. The case is a 43 yr-old man (at death). Onset of the disease was at his age of 10 when he had complained of leg pain. Since his age of 14, he had bone fractures of the lower extremities many times. At the age of 35, he was admitted to a hospital for the neurological examination. At that time, he showed exaggerated tendon reflexes and intension tremor of the upper extremities. He was euphoric and demented. His IQ was 31. Histological examination of biopsy specimen from the bone marrow revealed the typical membrano-cystic lesion. He had status epilepticus which was followed by comatous state for a week. The disease progressed gradually and he fell into decorticated state. He died at the age of 43. The total clinical course was 33 years. The brain weighed 680 g. Remarkable atrophy was observed in the whole brain. Loss of nerve cells in the upper layers of the cortex was marked. There were loss of myelin sheath and severe gliosis in the white matter. A part of the brain, liver and subcutaneous fat was frozen at the time of autopsy for the chemical examination. Quantitative determination of cholesterol, glycolipid, phospholipid, free fatty acid in the brain and liver, cholesterol, free fatty acid, triglyceride in the subcutaneous fat were carried out. Cholesterol was decreased about 33% in the cortex and 42% in the white matter in comparing with those of controls and the content of cerbroside in the white matter was about 1/3 of that of controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

[A case of neurogenic bladder complicated by an acute rash syndrome (measles?)].

A 24-year-old female patient was was admitted because of urinary retention, four days after the development of rash with fever to be diagnosed as measles by a doctor. Neurological examinations showed hyperesthesia in lower thoracic regions and increased deep tendon reflexes in lower extremities. Cystometric findings revealed an areflexic bladder with normal sensation. Cerebrospinal fluid examination showed mononuclear pleocytosis and slightly elevated levels of protein. There was no significant increase in serum measles antibody titer. She regained normal voiding by conservative treatment with an indwelling catheter for four days. The bladder motor paralysis was probably due to non-transverse myelitis in sacral spinal region. Neurological complications of measles are briefly discussed.

Adult↗
PubMed1988

Acute chest pain in an elderly woman.

A 79-year-old woman was admitted to hospital complaining of chest pain, increasing weakness, anorexia, hoarseness, headache and discomfort in the throat and jaws while eating. Physical examination, chest x-rays, serial electrocardiograms and cardiac enzymes were unremarkable. After admission she developed weakness and numbness in the left leg with urinary retention, decreased sensation to touch, weakness, increased tone, absent deep tendon reflexes and a positive Babinski sign on the left. Zeta sedimentation rate was markedly elevated at 0.63. Computerized tomographic head scan, myelography, echocardiography, barium swallow and meal, immunoglobulins, electrophoresis and other laboratory investigations were unremarkable. Repeat sedimentation rate was still markedly elevated three weeks later. A temporal artery biopsy confirmed the diagnosis of temporal or giant cell arteritis. Prednisone, 60 mg daily, was started.

Acute Disease↗
PubMed1988

[Epidural anesthesia in a patient with Friedreich's ataxia].

Friedreich's ataxia (FA), a hereditary disease with degenerative changes localized chiefly in the spinal cord and cerebellum, is characterized clinically by ataxia, absence of tendon reflexes, loss of proprioceptive sensation, and extensor plantar responses. There are only a few reports on anesthesia for patients with FA. General but not regional anesthesia is usually recommended because a persistent aggravation of symptoms is feared with regional anesthesia. We report a 31-year-old gravida 1 para 0 patient with FA who was admitted at the 20th week of gestation for induced abortion, curettage and tubal ligation. Familial FA was diagnosed at the age of 15, and since the age of 23 the patient had been confined to a wheelchair. As she strictly declined general anesthesia, epidural analgesia with 0.125% bupivacaine and morphine was used for 14 h, during which period induced abortion by prostaglandin was performed. This was followed by epidural anesthesia with 2% lidocaine for curettage and laparoscopic tubal ligation. A reduced dosage of local anesthetics, as commonly recommended during pregnancy, was used. Neurological consultation before and 1 day, 6 weeks, and 7 months after operation revealed no undue exacerbation of symptoms. Our case report suggests that epidural anesthesia can safely be administered to a patient with FA.

Abortion, Induced↗
PubMed1987

[A case of basilar artery fenestration with recurrent attacks of vertebrobasilar insufficiency].

Fenestration of basilar artery is an uncommon vascular anomaly that is usually an incidental product on autopsy or angiography. None of the cases in the literature had clinical symptoms associated with this anomaly except for subarachnoid hemorrhage when accompanied with saccular aneurysm. We report a rare case of the basilar artery fenestration associated with clinical symptoms without any aneurysm. A 71-years-old male, who had been treated for labile hypertension and had had recurrent attacks of vertigo, nausea, sometimes diplopia or unsteady gait, for 5 years, was referred to our hospital on Sept. 13, 1985. One day prior to admission, he suddenly felt diplopia and vertigo and unsteady gait. His family noticed he was dysarthric. On admission, he was alert and normotensive. He complained of dysesthesia on the right half of the perioral region and his right fingers. A neurological examination showed a mild weakness and hyperactive deep tendon reflexes on his right leg. His motor coordination was almost normal, but he was unsteady when he stood on one foot with his eyes closed. Laboratory examinations were normal except for an elevated serum uric acid level. A chest x-ray film showed a sclerotic change of aorta and mild cardiomegaly. Left ventricular hypertrophy was observed on his ECG. His CT scans showed multiple lacunae and mild brain atrophy. On cerebral angiography, his basilar artery (BA) had a fenestration almost in its total length that divided the BA, like a duplication, into two components with a smaller diameter than normal.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1986

Treatment of endemic goitre with iodine and thyroid hormones, alone or in combination. (Preliminary report).

108 patients with endemic nontoxic goitre have been treated in the field with thyroxine (T4), triiodothyronine (T3), and potassium iodide (KI), singly or in combination, or with placebo. After 6 months of continuous treatment, goitre size decreased significantly in the 7 actively treated groups, but not in the one treated with placebo. The combination of 150 micrograms T4 + 150 micrograms KI daily seemed the most effective treatment, both clinically and by its suppression of the 131I uptake and the TSH response to TRH, followed by 100 micrograms T4 + 25 micrograms T3 or 200 micrograms T4, but the difference from the other groups was not statistically significant. The increase in the pulse rate (PR) and the shortening of the photomotogram of the Achilles tendon reflex (PMG) were taken as indices of thyrotoxicity and side-effects of the treatment. There was no significant difference in the side-effects between any two of the active groups if effectiveness was also taken into account. The decrease in goitre size was not correlated to either the final serum T3 value achieved at the end of the treatment, or the thyroidal 131I uptake. There was, however, a weak but significant correlation between the decrease in goitre size and the TSH response to TRH. This casts some doubt to the concept that thyroid hormones decrease goitre size solely by suppressing the pituitary TSH release. Of the 30 patients treated with KI singly or in combination and studied in this respect, 8 developed autoantibodies against thyroglobulin and/or the thyroidal microsomal antigen compared to 1 of 22 not receiving KI (P = 0.08).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1987

[An autopsy case of syringomyelia associated with Chiari malformation and basilar impression].

The authors report one autopsy case of syringomyelia associated with Chiari malformation and basilar impression. The pathogenesis of syringomyelia in our case is discussed. This 37-year-old man complained of progressive difficulty in swallowing and walking for two years. He had noticed dysarthria for six months before admission. (Examination) Neurological examination showed dysarthria, down beat nystagmus, disturbance of IXth nerve, Xth nerve and XIth nerve, and cerebellar ataxia. Deep tendon reflexes were hyperactive in the upper and lower extremities. Babinski's sign was positive bilaterally. Neuroradiological examination demonstrated basilar impression and Chiari malformation. (Operation) Suboccipital craniectomy and laminectomy of upper cervical vertebra were performed with dural plasty. Postoperatively he acquired some improvement, but soon after he was worse. He died of respiratory disturbance. (Postmortem examination) Though the central canal was obliterated at the C4 level, the syrinx extended from the C5 to Th7 level. From the C5 to C8, the syrinx was present in the areas of central gray matter, extending into the left dorsal horn, where it communicated with subarachnoid space. Furthermore, the abnormal vessels were noticeable around the syrinx. At the Th2 level, they were also shown in central grey matter where no syrinx existed. (Conclusion) The etiology of syringomyelia in our case was not explained by Gardner's hydrodynamic theory. We suggested that intramedullary abnormal vessels played an important part for the formation of the syringomyelia.

Adult↗
PubMed1986

[A case of Isaac's syndrome--continuous muscle fiber activity syndrome].

A 34-year-old woman noted difficulty of gait initiation, then dilated finger opening and hyperhidrosis appeared. Her stature was a muscular habitus, and muscle stiffness and myokymia were found in all muscles of the extremities. Her stiffness persisted during sleep. Her calf muscles were large and a contracture was noticed in ankle joints. There was no evidence of wasting and weakness. A remarkable delay in voluntary relaxation of the contracted muscles without percussion myotonia was recognized. Tendon reflexes of lower extremities were absent. Laboratory examination revealed elevation of CPK, LDH, myoglobulin, aldolase and basal metabolic rate (BMR). An extraband of CPK isoenzyme between MB and MM fraction was observed. The thin layer gel filtration technique and immunofixation technique showed that this extraband was complexes of CPK and IgA, and light chain of the CPK linked IgA was lambda type. All other laboratory tests were normal for the following: urinalysis, ESR, a blood count, liver function, kidney function, glucose, rheumatoid factor, CRP, thyroid function, parathyroid function, serum electrolytes, ECG, EEG, cranial CT, without slight elevation of IgA, and CSF protein. In needle EMG and surface EMG spontaneous discharges were recorded at rest. These discharges consist of normal motor unit potentials, doublets, and triplets in needle EMG. The discharges were markedly reduced after the median nerve block with xylocaine. In needle EMG, myotonic discharge was not observed. Nerve conduction velocities were within normal ranges. According to these data, she was diagnosed as having Issacs' syndrome (continuous muscle fiber activity syndrome). Carbamazepine, 200 mg daily was administrated and showed a dramatic reversal of the symptoms.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

[Hydrocephalus in Paget's disease--a case report].

A case of Paget's disease in an elderly female who had a favourable evolution following ventriculoperitoneal (V-P) shunt is reported. On May 28, 1983, a 52-year-old female was transferred and admitted to us from the Dept. of Neurology because of headache in the occipital region and ataxic gait. On admission, neurological examinations revealed remarkably increased tendon reflexes, ataxic gait, and mild dementia. Headache was also observed, but urinary incontinence was not present. Skull X-ray showed "cotton wool appearance", which was characteristic of Paget's disease. On chemical analysis of blood and urine, serum Al-P and urinary OH-proline level were elevated, which established a diagnosis of Paget's disease. Triventricular dilatation was found on CT scan, and neck tomography showed basilar impression. After admission, the patient was treated with calcitonin, but it was interrupted because of side effects such as nausea and vomiting. Then she gradually took a turn for the worse, particularly dementia became severer. On July 25, 1983, V-P shunt was performed. After operation, "soft landing maneuver" was employed, namely the intraventricular pressure was checked and was gradually lowered with external CSF drainage system for 7 days. Thereafter the patient's head was elevated gradually from supine to sitting position through 7 days. Her hospital course after operation was that of gradual improvement. The purpose of this maneuver was to prevent sudden change of intraventricular pressure that causes aggravation of basilar impression and sudden respiratory arrest.

Cerebrospinal Fluid Shunts↗
PubMed1986

[Myxopapillary ependymoma of the filum terminale with a holocord cyst: a case report].

This paper describes a case of myxopapillary ependymoma of the filum terminale with a holocord cyst. A fifteen-year-old boy was admitted because of dysarthria, dysphagia and tetraparesis. He also suffered from severe lumbago and ankle pain for three years. On admission his vital signs were stable and neurological examination revealed lower cranial nerve palsies (from 9th through 12th), tetraparesis, bilateral impairment of vibratory and position sense of the lower extremities and urinary incontinence. All deep tendon reflexes were hypoactive bilaterally. Babinski reflex and Lasègue sign were negative bilaterally. The spine roentgenograms revealed widening of the interpedicular distance from C 1 to L5 except L2, 3 vertebrae. Lumber puncture at the L 1-2 interspace revealed a cyst at the site and the protein content of the cyst fluid was 2400 mg/dl. MRI demonstrated a syrinx extending from the medulla to the entire cervical cord. From these results, it was concluded that the medulla and the entire spinal cord were occupied by the tumor and some parts of the lesion were cystic. First Operation: After a suboccipital craniectomy and a laminectomy from C 1 to Th 2, the medulla and the cervical cord were decompressed by evacuating the cyst at the 4th cervical segment. After the first operation, the C 1-2 myelography and MRI confirmed that the medulla and the spinal cord above the Th 11 vertebra were decompressed and the lower end of the cyst was extending to the Th 11 level. Second Operation: After a laminectomy from Th 12 to L4, a solid tumor arising from the filum terminale was completely removed.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1986

[A case of polyradiculoneuropathy associated with diffuse arterial narrowing].

A 32-year-old female was admitted complaining of pain over the whole body and dysesthesia in all extremities. On admission, physical examination revealed hypertension, tachycardia, abdominal distension and urinary retention. Neurological examination revealed sensory impairment over the whole body and mild muscular weakness with absent deep tendon reflexes. Abdominal roentgenogram showed gaseous distension of the bowels. CT scans showed low density areas on the bilateral parieto-occipital lobes. CAG showed diffuse narrowing of the cerebral arteries. Laboratory examinations showed an albumino-cytologic dissociation (cells; 21/3mm, prot.; 78 mg/dl) of the cerebrospinal fluid and increased levels of norepinephrine (214 micrograms/day) and epinephrine (16.1 micrograms/day) in the urine. Motor nerve conduction velocities of the median nerves was 42.8 m/sec in the right and 50.0 m/sec in the left. The autonomic function tests revealed hyper-responsiveness to 10 mg of phentolamine and low baroreflex sensitivity. Within 2 months, most symptoms improved. Repeated CT scans showed no abnormality, while CAG showed only mild arterial narrowing. This case was diagnosed as having acute autonomic and sensory neuropathy which was a subtype of acute polyradiculoneuritis. Occult encephalitis or autonomic dysfunction was considered to contribute to the peculiar findings on CT and CAG.

Adult↗
PubMed1986

Severe neonatal centronuclear (myotubular) myopathy: an X-linked recessive disorder.

Prenatal onset and rapidly fatal course of centronuclear myopathy are described in four male newborns including two brothers. Diagnosis was established by muscle biopsy within the first week of life in two and at autopsy in the two other patients: Central nuclei, central aggregation of oxydative enzyme activity in the majority of muscle fibers and type 1 fibre hypotrophy were demonstrated. Prenatal manifestation included polyhydramnios, reduced fetal movements and breech presentation. All four newborns developed respiratory insufficiency requiring artificial ventilation immediately after birth. Severe muscular weakness and hypotonia as well as hardly elicitable grasping, deep tendon reflexes and Moro response were noticed. Additional findings included high arched palate, joint contractures, thin ribs, lung hypoplasia, abundant skin and cryptorchidism. In two families, the pedigree contains other affected males, suggesting X-linked inheritance. Seven female carriers were clinically healthy and one of them showed normal muscle histology. Fourteen previously published neonatal cases of centronuclear myopathy are reviewed and compared with our findings. This severe perinatal form of centronuclear myopathy has to be considered in male fetuses and newborns with polyhydramnios and respiratory failure due to muscular weakness or in infants who died of unexplained postnatal asphyxia. Diagnosis should be established by muscle biopsy.

Genetic Carrier Screening↗
PubMed1986

[A case of dural arteriovenous malformation with bilateral thalamic infarction].

A 59-year-old man was admitted because of frequent vomiting and obtundation in February 1982. Neurological examination on admission revealed only slight impairment of consciousness. Papilledema, meningeal irritation sign and paralysis were not elicited. The plain CT scan was normal, but the CT scan with contrast material showed patchy enhancement in the left temporal lobe and around the third ventricle. Cerebral angiography showed a dural arteriovenous malformation (dural AVM) in the left transverse sinus fed by the left occipital artery, and the retrograde flow into the straight sinus. By the third day following admission, the level of consciousness became alert. The patient did not complain of headache, bruit and visual disturbance. He showed mild disorientation and memory disturbance. But his ordinary daily-living was independent. In August 1982, the patient gradually became inactive and apathetic. At times he lay in bed with moving his eyes, swallowing foods. At other times, he lay in bed with closing his eyes, immobile, and unresponsive except to strong painful stimuli. The patient was incontinent and required nursing care. During three month periods, the patient progressively became somnolent, speechless and immobile. Eventually, he was in a state of akinetic mutism. The patient became unresponsive. The state of consciousness fluctuated within a narrow range. The pupils were isocoric and did not react to light. He sometimes moved his eyes horizontally, but the vertical eye movement was limited. Deep tendon reflexes were hyperactive with Babinski reflex bilaterally. Passive mobilization of extremities revealed hypertonic. The CT scan disclosed the bilateral symmetrical infarction of the thalamus.(ABSTRACT TRUNCATED AT 250 WORDS)

Arteriovenous Malformations↗
PubMed1986

[Chronic toluene intoxication and hyperkinésie volitionnelle].

Hyperkinésie volitionnelle is one of the involuntary movements discriminated from intention tremor. It occurs idiopathically and with cerebral infarction, head trauma, brain tumors, multiple sclerosis, hepatolenticular degeneration and polyneuropathy. Here, we report a case of toluene intoxication presenting hyperkinésie volitionnelle. A 28-year-old painter noticed a tremor of the upper extremities on December 1979. The tremor occurred both in posture and in voluntary movements. The tremor gradually developed and appeared in the legs in May 1980. Slight titubation of the trunk and head was marked in sitting posture. He showed staggering of gait. On August 1980, he exhibited slurred speech. He was admitted to the Department of Neurology of Chiba University Hospital on January 19th, 1981. Neurological examination revealed slight mental deterioration, pendular nystagmus, bradylalia, 4-5 c/s violent postural tremor of the upper extremities, action myoclonus, head and truncal titubation, mild leg tremor in sitting posture. The tremor increased terminally on finger to nose testing, and showed fast, coarse, convulsive movement (movement oppositionniste). But there was no dysmetria. The involuntary movements, above mentioned, were summarized as hyperkinésie volitionnelle. Muscle tone was hypotonic. Muscle weakness and atrophy were not seen. Deep tendon reflexes were all exaggerated, but there was no pathological reflex. He showed wide-based ataxic gait. Sensory and autonomic functions were normal. Blood, urine and cerebrospinal fluid analysis appeared normal. Electroencephalography showed 40-50 microV, 9-10 c/s alpha waves with a few fast waves.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Stiff-man syndrome with spinal cord lesion.

An autopsy case of stiff-man syndrome is presented. The patient was a 54-year-old man who had suffered from fluctuating rigidity and tonic spasm of the trunk and leg muscles for three years. These symptoms were induced by emotional stress, strain at voiding and other external stimuli. Physical examination revealed stiffness of the neck, trunk and legs without obvious muscle weakness or atrophy. Deep tendon reflexes were hyperactive, while sensation was normal. EMG showed the stiffened muscles to have continuous motor unit activity which was decreased by myoneural block, spinal anesthesia, diazepam or sleep. Administration of diazepam (60 mg daily) gave some relief of the stiffness for several days. However, respiratory arrest suddenly occurred. Although the patient was resuscitated, he died nine days after this episode. Examination of the spinal cord revealed loss and degeneration of nerve cells with marked gliosis in the medial motor nuclei of the anterior horns. A symmetric degeneration in the bilateral anterior columns which has never been described as a spinal cord lesion in the stiff-man syndrome was also seen.

Brain↗
PubMed1985

Vinca alkaloid-induced cardiovascular autonomic neuropathy.

To determine the incidence of vinca alkaloid (VA)-induced cardiovascular autonomic neuropathy (CAN), neoplastic patients were studied. Thirty-three of them were receiving chemotherapy regimens including VAs, and 30 were receiving chemotherapy without VA and were considered controls. Abnormal variation in blood pressure on standing, heart rate during deep breathing, and heart rate on standing was found in 27 (82%), 16 (48%), and 16 (48%) patients receiving VA versus nine (30%; P less than 0.01), three (10%; P less than 0.05), and one (P less than 0.001) controls, respectively. Of 198 tests performed, 100 were abnormal in patients receiving VA (51%) versus 33 of 180 tests in the controls (18%; P less than 0.001). Although abnormal clinical or electrocardiographic tests for CAN appeared significantly more frequently in patients who received high doses of VA (P less than 0.01), their incidence was not significantly different in patients greater than or equal to 60 years of age, in those who received doxorubicin, or in those who showed abnormal deep tendon reflexes. The consequences of VA-induced CAN might be especially important for potentially curable cancer patients.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1985

[Infantile myositis].

An eleven-months-old boy with motor developmental delay, muscle weakness, hypotonia and normal tendon reflexes was diagnosed as having infantile polymyositis, histologically with a vasculitis component. Corticosteroid treatment was successful. At the age of 5 years he showed a normal motor pattern.

Humans↗
PubMedDate not supplied

[Globoid cell leucodystrophy (Krabbe's disease). Peripheral nerve lesion (author's transl)].

Morphological study of peripheral nerves in two patients with globoid cell leucodystrophy (Krabbe's disease) demonstrates: 1degree segmentary demyelination; 2degrees marked loss of large (8-10 micra) myelinated fibres; 3degrees significant increase of the mean transverse fascicular area by proliferating collagen fibres; 4degrees electron-microscopic signs of remyelination with small onion-bulb formations. These findings can explain clinical features such as the disappearance of the deep tendon reflexes, the gradual transition of hypertonia into combined hypertonia-hypotonia and the concomitant slowing of nerve conduction velocity. The ultrastructural study reveals the presence of large and small inclusions which are either located within lysosomes or free in the cytoplasm of Schwann cells and fibroblasts. The inclusions are probably consequences of the disturbed metabolism of cerebrosides. Their appearance is sufficiently specific in order to allow a diagnosis of Krabbe's disease.

Axons↗