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PubMed1989

[A case of acute spinal epidural hematoma with spontaneous resolution and its MRI].

A case of non-traumatic spinal epidural hematoma (SEH) with spontaneous resolution was reported. A 80-year-old woman was admitted to our hospital for her paraplegia of acute onset. She had had no specific previous history, and she did not either receive any drug or suffer from hypertension. On admission, general status was unremarkable. Flaccid paralysis of lower extremities and bilateral sensory disturbance of all modalities below the level of Th4 were observed. Deep tendon reflexes were normal in upper extremities, while absent in lower extremities. Babinski's sign was not elicited. From the findings of CT and metrizamide CT myelography, SEH of ventral type was presumed. MRI revealed hematoma compressing spinal cord over two vertebral segments, and widely spreading even to C7 rostrally and to Th10 caudally. Urgent surgical intervention was taken into consideration, but was not performed because of her rapid improvement: sensory disturbance alleviated from day to day, and she became able to walk within the 3rd day of hospitalization. Almost complete recovery from motor and sensory dysfunction was achieved in about 7 days after admission. Only 4 cases of spontaneous recovery of SEH have been reported so far, and this patient is the 5th such case. Although CT and metrizamide CT myelography are useful in diagnosing SEH, MRI is also proved to be an accurate and efficacious method for evaluation of its size, location and extent in the spinal canal.

Acute Disease↗
PubMedDate not supplied

[Anderson's disease. Clinical and morphologic study of 7 cases].

Anderson's disease is a rare autosomic recessive condition involving the transport of fat through the intestinal mucosa, which could be due to a defect in the intestinal form (B48) of apolipoprotein B. Isolated cases and one important series only have been reported. We wish here to complete the description of the disease. Seven children (age 6 months to 13 years at time of diagnosis) were followed for one month to 15 years. They presented with a malabsorption syndrome, malnutrition, fatty diarrhea (steatorrhea 4-18 g/24 h), failure to thrive (height -1 to -5.5 SD for age) and sometimes disappearance of deep tendon reflexes. Biologically they had signs of malabsorption, hypocalciuria, osteoporosis, low serum iron, decreased levels of vitamins A and E, and hypo-alpha- (50-127 mg/100 ml) and beta- (73-175 mg/100 ml) lipoproteinemia due to decreased levels of plasma cholesterol (40-70 mg/100 ml), and phospholipids (34-67 mg/100 ml); apolipoproteins A1 (26-69 mg/100 ml and B (21-44 mg/100 ml) were also low. After a fatty meal, triglycerides and apolipoproteins did not increase and chylomicrons did not appear. Jejunal biopsies showed the characteristic aspect of enterocytes loaded with lipid droplets. On electron microscopy, these fat droplets were seen in the cytoplasm but neither in the endoplasmic reticulum and the Golgi complex nor in the intercellular spaces. They did not appear to be enclosed in membranes and differed from chylomicrons by their size and density. The disease could thus be due to an abnormal apolipoprotein B48, which would prevent its binding to triglycerides and thus the formation of chylomicrons.

Adolescent↗
PubMed1989

[CT evidence of high density area in bilateral striatum secondary to anoxia].

We recently observed a patient in whom basal ganglia calcification (BGC) was demonstrated on sequential CT scans only 9 days after the anoxic episode. A 58-year-old woman had a history of diabetes mellitus for 23 years for which she was treated with insulin. She had a operation for retinal detachment under local anesthesia. Two days after the operation, she developed dyspnea, and was referred to our department. She was intubated, and respiratory support was begun. On neurological examination, she was semicomatose, and intermittent spontaneous movements involved in all extremities. The pupils were 3 mm in diameter, equal and responsive. Full doll's eye responses were obtained both horizontally and vertically. Deep tendon reflexes were hyperactive bilaterally without ankle jerks and extensor plantar responses. Arterial blood gas levels revealed a PaO2 of 49 mmHg, PaCO2 38 mmHg: pH 7.16. Serum Ca, P, Mg, Al-p and parathyroid hormone levels were normal. The EEG was isoelectric. Although the initial CT scan was normal, the subsequent CT scan 9 days later showed extensive high density change of the striatum, which was assumed to be BGC due to anoxia was briefly discussed.

Basal Ganglia Diseases↗
PubMed1989

[Spastic paraplegia in Sjögren's syndrome associated with mixed connective tissue disease (MCTD)--a case report].

A case of spastic paraplegia in Sjögren's syndrome associated with mixed connective tissue disease is reported. In this 49-year-old woman spastic gait and arthralgia developed at the age of 23 years and progressed chronically. On neurologic examination, supranuclear paresis of facial nerve was observed. Deep tendon reflexes were hyperactive in the jaw, upper and lower extremities. Serological tests showed that anti-nuclear, anti-RNP, and anti-SS-A antibodies were positive. Spinal fluid analysis showed that rate of de novo central nervous system (CNS) IgG synthesis was increased, and C3/C4 ratio was elevated. CT scans of the brain showed calcifications at bilateral basal ganglia, dentate nucleus and cerebellar vermis. An electroencephalogram revealed diffuse slowing, and 123I-IMP brain scans revealed decreased cerebral blood flow. MRI of brainstem and cervical cord were normal. These findings suggested that corticospinal tracts upper the brainstem were severely affected, and that there were multifocal latent lesions in the CNS. Mechanisms of the CNS involvement were supposed to be both autoimmune abnormality in the CNS, and vascular impairment.

Central Nervous System Diseases↗
PubMed1989

[A nosological study of a patient showing ataxia & lower motor neuron involvement].

A sporadic case of spinocerebellar degeneration with prominent involvement of the motor system has recently been encountered. A 54-year-old man without family history noticed speech disturbance at the age of 46 and weakness in his right hand the following year. The muscle weakness and atrophy were slowly progressive and made walk impossible at the age of 50, when his dysphagia increased. At the age of 54, he was admitted to our hospital when neurological findings revealed marked amyotrophy of general skeletal muscle and tongue with fasciculation. Deep tendon reflexes were decreased. Cerebellar ataxia was impossible to evaluate because of profound muscle weakness. And sensory disturbance was suspected in the distal portion of the lower extremities. CT scan revealed progressive atrophy of the brain stem and cerebellum. The patient died at the age of 54 due to CO2 narcosis. The clinical course was 8 years. A summary of the pathological findings was as follows: 1) Marked neuronal loss of the anterior horn of the spinal cord and motor cranial nerve nuclei except for oculomotor nuclei, with mild degeneration of pyramidal tract below lumbosacral level. 2) Degeneration of cerebellipetal system, spinocerebellar tract, Clarke's column and the middle root zone and cerebellifugal system, dentate nucleus, superior cerebellar peduncles, and red nucleus. 3) Mild degeneration of pontine nuclei, inferior olivary nuclei, pontine transverse fibers, the middle and inferior cerebellar peduncles, cerebellar white matter and Purkinje cells as in OPCA.(ABSTRACT TRUNCATED AT 250 WORDS)

Amyotrophic Lateral Sclerosis↗
PubMed1989

[A case of recurrent multiple cerebral infarctions with protein C abnormality].

A 38-year-old man of recurrent episodes of multiple cerebral infarctions with protein C abnormality was reported. He had six episodes of visual disturbance within a year. The neurological examination revealed bilateral visual loss and impaired visual field except for small central area. However, there were no abnormalities in the deep tendon reflexes and muscle strength of all extremities and cerebellar examinations. CT scan revealed multiple low density areas in the bilateral posterior lobes, and cerebral angiography demonstrated the severe stenosis of the ganglionic portion and the supraclinoid portion of the right internal carotid artery. Plasma levels of antithrombin-III activity, plasminogen activity, protein C activity, protein C antigen and protein S antigen were 105, 106, 28, 166 and 120%, respectively. Because only protein C activity decreased markedly, a diagnosis of protein C abnormality was established. We started warfarin therapy under the administration of concentrates of factor IX complex, since then there has been no cerebral accident.

Adult↗
PubMed1989

[Effect of surgery on neurological involvement caused by a lumbosacral radicular syndrome].

Results of neurological assessment one year after surgical treatment of herniated lumbar intervertebral disc and lumbar stenosis are reported in 443 patients. Follow-up was performed during one year after operation. Preoperatively, surgeons found motor loss more frequently than patients, (28 and 12% respectively) and, postoperatively, motor loss was still present in 25% and 24%, respectively, of these cases. The operation had caused motor loss in 5% and aggravated motor loss in 3%. Sensibility was reported as abnormal one year after surgery by both patients and surgeons in one-third of the cases. Sensory loss, considered by the patient to have been caused or aggravated by the operation, occurred in 15% of the cases and in 12% of these the surgeons agreed. Preoperatively, unilaterally diminished knee and Achilles tendon reflexes were found in 9% and 42% respectively; one year after surgery, these had recovered in 65% and 57%, respectively. Surgery caused or aggravated unilaterally diminished knee or ankle jerks in 3% and 10%, respectively.

Adult↗
PubMed1989

[An autopsy case of carcinomatous sensory neuropathy associated with gastric adenosquamous carcinoma].

A 61-year-old man was admitted on May 1986 with complaints of hypesthesia and pain in the both legs, and of progressive difficulty in walking. Physical examination was unremarkable. On neurological examination, deep tendon reflexes were decreased in all extremities without pathological reflexes. Vibration sense was decreased severely at the medial malleolus and moderately at the anterior superior iliac spine. Joint sensation of the toes was moderately decreased. Light touch, temperature discrimination, and pinprick sensation were slightly decreased on fingers bilaterally and distal to the middle part of both legs. Muscle strength was normal. His gait was unsteady and Romberg's sign was positive. Finger to nose test and heel to knee test were mildly disturbed bilaterally. The sural nerve action potential was not elicited on electrical stimulation. Laboratory studies for malignancy showed gastric cancer. Only July 4, he underwent subtotal gastrectomy. Histologically it showed adenosquamous carcinoma. Postoperatively gait disturbance and pain in both legs improved slightly. Peak latencies of P2 of SEP following right and left posterior tibial nerve stimulation were 47. 9 msec and 48.8 msec on February 14, and 44.5 msec and 43.9 msec on October 6, 1986, respectively, and their postoperative shortening was evident. He died of multiple liver and lung metastasis of the gastric cancer in November 28, 1986. At autopsy, tumor metastasis were noted in liver, lung and perigastroduodenal and retroperitoneal lymph nodes.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenocarcinoma↗
PubMed1989

Electroretinographic findings in inherited ataxias.

Electroretinogram was performed in 18 patients with inherited ataxias. Eight had Friedreich's disease, 9 autosomal dominant cerebellar ataxia and one early onset cerebellar ataxia with retained tendon reflexes. Abnormalities were found in one patient for each group. The most frequent were decreased b-wave amplitude in photopic and scotopic conditions and prolonged implicit time.

Adolescent↗
PubMed1989

Influence of thyroid hormone supply on EEG frequency spectrum.

In 5 patients after total thyroidectomy followed by radioiodine ablation the frequency analysis of EEG based on fast Fourier transformation was performed and the results obtained during hypothyroid state and after the substitution treatment with thyroid hormones were compared. During the hypothyroid state the most remarkable finding was the increase of percentage representation of fast frequencies in beta 1 and beta 2 bands, while such values in alpha band including a dominant frequency in that band were reciprocally decreased. After the period of treatment with triiodothyronine during which clinically euthyroid state has been achieved (i.e. decrease of Achilles tendon reflex time, decrease of TSH and of T3 level) no significant changes in the distribution of EEG frequencies spectrum were found, but in all patients a dominant frequency in alpha band was increased at least for 1 Hz. Only after the treatment with thyroxine (Eltroxin Glaxo) the interrelations between individual frequencies of EEG spectrum returned to the normal range and a further increase in dominant alpha frequency was found. The correlation between a dominant frequency in alpha band and thyroxine level in serum was highly significant. These findings are in agreement with our previous observations in 43 subjects where a dominant alpha frequency in healthy controls was always higher than that in hypothyroid subjects and was significantly related to T4 level. The findings of continuing EEG signs of brain hypothyroidism even after achieving of clinical euthyroidism and normal peripheral parameters under increased serum T3 and low T4 level are in full agreement with experimental observations on the importance of local deiodination of T4 in brain tissue and on the risk of hypothyroxinemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

[Paroxysmal itching and magnetic resonance imaging of the spinal cord in multiple sclerosis].

In three women with multiple sclerosis, paroxysmal itching occurred. We were able to detect the spinal segment lesions corresponding to the dermatome of paroxysmal itching by magnetic resonance imaging (MRI) in them. Case 1. A 38-year-old woman was admitted with chief complaints of tingling sensation in the left side of the body, left hemiparesis and paroxysmal itching in the neck and left upper extremity. Examination on admission revealed left hemiparesis, mildly exaggerated deep tendon reflexes in the left upper and lower extremities, positive Lhermitte's sign. Superficial sensation was decreased and dysesthetic below the left C3 segment. Vibration and joint sense were moderately decreased in the left upper limb. Painful tonic seizure-like attack occurred in the neck bilaterally. Paroxysmal itching occurred in the neck and left upper extremity corresponding to the cervical spinal segments bilateral C3, left C4 to C6. MRI revealed multiple high signal intensities in the white matter of the cerebral hemispheres, the medullo-cervical junction and the cervical segment C3 to C4 in T2-weighted spin-echo images. The C3 to C4 lesion was found in the left dorsal area of spinal cord in axial image. High signal areas of cervical cords on T2-weighted spin-echo images were reduced in response to adrenocorticosteroid therapy, and paroxysmal itching disappeared. Case 2. A 24-year-old woman complained chiefly of mild tetraparesis and left hand clumsiness. On admission, she had right central facial palsy, mild weakness of all limbs, painful tonic seizure of left upper limb, positive Lhermitte's sign and bilateral Babinski sign. Superficial sense was mildly decreased and dysesthetic in left upper extremity.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Early onset hereditary spinocerebellar ataxia: an autosomal recessive disorder distinct from Friedreich's ataxia.

The important clinical features of seven patients with an early onset slowly progressive heredofamilial spinocerebellar degenerative disorder of probably autosomal recessive inheritance included limb ataxia, retained and/or exaggerated tendon reflexes (biceps and knee), pyramidal weakness of lower limbs and normal sensory action potentials. This rare disorder is probably distinct from Friedreich's ataxia and carries a better prognosis.

Adolescent↗
PubMed1989

[Chronic Guillain-Barré syndrome (diagnostic and therapeutic possibilities)].

The authors survey the clinical features and therapeutic results of their patients with chronic inflammatory polyneuropathy. There was an antecedent virus infection in the case history of 5 out of 7 patients. In one patient the chronic polyneuritis developed in association with previously verified SLE, in an other one the autopsy has proved giant lymphadenopathy. The symptoms and signs have evolved slowly in 6 patients, one patient relapsed in 4 months after the first acute attack. The initial and main symptom was the hypotonic muscle weakness of lower extremities. All of the patients mentioned paresthesias and on the lower extremities of 4 patients even hypesthesias of distal type might be revealed. The tendon reflexes were always very slow or absent. In the CSF the classical changes, excess of protein content with normal cell count were found. The electroneurography has shown increased distal latencies and reduced motor and sensory nerve conduction velocities. The steroid treatment and in 2 patients the plasmapheresis were successful, however the recovery was always incomplete and residual disabilities persisted. The electrophysiological and CSF findings did not change parallel with the relief of clinical symptoms and signs.

Adult↗
PubMed1989

Hereditary motor-sensory neuropathies. Charcot-Marie-Tooth syndrome.

The Charcot-Marie-Tooth (CMT) syndrome is also referred to as hereditary motor-sensory neuropathy (HMSN). It is not a single disease but has a multitude of genetic causes. The typical clinical characteristics are distal muscle weakness and atrophy, depressed tendon reflexes, often slow motor NCV, and the frequent finding of other similarly affected relatives. The most common variant of this syndrome is HMSN-I showing autosomal dominant inheritance, markedly slow motor NCV and nerve hypertrophy. One form of HMSN-I is linked to the Duffy locus on chromosome 1. There are numerous other varieties of HMSN including other autosomal dominant conditions such as HMSN-II (with nearly normal motor NCV) and several types of familial amyloid neuropathy (with specific amino acid substitutions in transthyretin); autosomal recessive conditions such as HMSN-III (Déjérine-Sottas hypertrophic neuropathy of childhood) and Refsum's disease (defect of phytanic acid metabolism); and conditions produced by mutations on the X chromosome such as X-linked HMSN, Fabry trihexoside storage disease, and adrenomyeloneuropathy. The known biochemical abnormalities, chromosomal locations, clinical findings and genetic counseling of these disorders are reviewed.

Charcot-Marie-Tooth Disease↗
PubMed1989

[Progressive spinal muscular atrophy and parathyroid adenoma. Clinico-pathologic study of a case].

A 82 year-old man died 6 years after the onset of a progressive spinal muscular atrophy. Post-mortem examination disclosed a parathyroid adenoma. Weakness and wasting were prominent in the proximal lower limbs. There were no fasciculations. Involvement of the medulla was mild and late. These clinical features were also present in 16 reported cases, which were improved by treatment of primary or secondary hyperparathyroidism. Our patient differs by the involvement of the hand muscles and the loss of tendon reflexes. Neuropathological study, as in one other reported case, showed a loss of anterior horn cells. Such cases underline that calcium metabolism must be studied in syndromes of spinal muscular atrophy.

Adenoma↗
PubMed1989

[Effect of sinestrol on the course of the myodystrophic process in progressive Duchenne muscular dystrophy].

Therapeutic effect of sinestrol was investigated in 15 patients with progressive muscular dystrophy of Duchenne (PMDD) aged 7 to 10 years, at stage II of the disease. The drug was given orally 1 mg twice a day for 3 weeks. Control group consisted of 14 patients with PMDD aged 7 to 9 years. By the end of the course a several relief of motor constraint was noted in 10 patients with functional tests improved, tendon reflexes increased. The results of clinico-electromyographic investigation performed 6 months after the sinestrol withdrawal evidenced progressive course of the disease, though its rate was significantly lower in sinestrol-treated group. The treatment did not produce considerable changes in the baseline hormonal profile (gonadotropins, prolactin, sexual steroids).

Administration, Oral↗
PubMed1989

[Causalgia in the upper limbs following neck trauma: existence of widespread dysfunction of sympathetic postganglionic fibers].

The functions of autonomic nervous system were systematically evaluated in a case of causalgia in the upper limbs after neck trauma. A 14-year-old boy had had hard blow on his nucha in a rough fight. After one week, a sustained burning pain, swelling and skin color change developed in the left upper limb. These symptoms also appeared in the right upper limb after 6 weeks. The physical examinations disclosed edema, reddish moist skin, and atrophic nail in the upper limbs. The neurological examinations showed a radiating pain to the upper limbs caused by the neck movement or pressure on the supraclavicular fossae, weakness of the upper limbs and left lower limb, and loss of sensation in the 5th to 8th cervical and first thoracic dermatomal segments. Deep tendon reflexes were diminished in the upper limbs and exaggerated in the lower limbs. Neither Horner syndrome nor sphincter disturbance was observed. He was diagnosed as being the cervicothoracic radiculopathy and cervical myelopathy due to the mechanical force. The burning pain disappeared with oral administration of guanethidine. On the examinations of the autonomic functions, the sweating response to the thermal stimulation was absent above the 5th thoracic dermatomal segment. The sweating response to the intradermal acetylcholine was decreased in the second and third thoracic dermatomal segments. The systolic hypotension with increasing pulse rate occurred on standing. The reactive elevation of the blood pressure to the intravenous tyramine was absent. The excessive elevation of the systolic blood pressure was induced by the subcutaneous injection of epinephrine. These results indicated the dysfunction of the sympathetic postganglionic sudomotor and vasomotor fibers.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1989

Magnesium therapy of cardiac arrhythmias in critical-care medicine.

A common complication of critically ill patients is cardiac tachyarrhythmia. The role played by magnesium is not well appreciated. Well-documented cases indicated that magnesium may be effective in controlling the rhythm when conventional methods fail. The following tachyarrhythmias respond favorably to magnesium: (1) intractable ventricular tachycardia and fibrillation, whether hypo- or normomagnesemic, (2) torsades de pointes, (3) digitalis-toxic ventricular tachyarrhythmia, (4) multifocal atrial tachycardia and (5) hypomagnesemic atrial tachyarrhythmia. It is recommended that 10-15 ml of 20% MgSO4 be infused over 1 min, followed by 500 ml of 2% MgSO4 over 5 h. A second 500 ml over 10 h may be necessary. Renal failure, disappearance of deep tendon reflex, rise in serum Mg above 5 mEq/l, drop in systolic blood pressure below 80 or drop in pulse below 60 contraindicate the continued use of magnesium. If serum potassium is at or falls below 4.0 mEq/l, 20-40 mEq/l KCl should be added. Magnesium deficiency can be confirmed by a low serum level or by a greater than 50% retention of administered magnesium. The causes of magnesium deficiency can be remembered under 10 DS: (1) Diarrhea and gastrointestinal losses, (2) Diuretics and renal losses, (3) Diabetes and endocrine causes, (4) Dietary lack, (5) Diverted to free fatty acids, (6) Drugs such as cisplatin, (7) Drinking alcohol to excess, (8) Delivery with toxemia, (9) Decompensated heart, lungs or liver and (10) Denuded skin, such as burns.

Arrhythmias, Cardiac↗