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PubMed1992

[A case of sarcoid polyradiculopathy with nerve roots swelling demonstrated by myelography].

A 62-year-old woman was admitted to our hospital because of tingling numbness in the trunk and upper extremities. She was well until 18 days earlier, when she began to feel tingling numbness on the ulnar side of the left arm. During the next two weeks it spread gradually over the trunk and ulnar side of the bilateral arms. She had also progressive difficulty in taking hold of objects. On neurological examination she was alert and cooperative with normal articulation. The neck was supple. The cranial nerves were intact. Superficial sensation was bilaterally hypesthetic in the distribution from the 7th cervical through 12th thoracic segments. Mild weakness was distally noted in the upper extremities. Deep tendon reflexes were reduced or absent without laterality. Plantar responses were bilaterally flexor. Coordination and gait were normal. Routine laboratory examinations including blood counts, blood chemistries and urinalysis were unremarkable. Serum angiotensin converting enzyme (ACE) was slightly elevated. A lumbar puncture yielded clear, colorless cerebrospinal fluid (CSF) containing 22 white cells/mm3 and protein of 106 mg/dl. Conventional nerve conduction studies were normal. F-wave conduction studies revealed elevated F-ratios for the upper and lower extremities. Studies of short-latency somatosensory evoked potential showed mild prolongation of N13 recorded after stimulation of the right median nerve. An X-ray film of the spine was unremarkable except for mild narrowing of the C5-6 intervertebral disk space. Postcontrast magnetic resonance imaging of the spine with gadolinium-DTPA was unrevealing as well as a precontrast study. A myelogram disclosed enlarged lateral filling defects corresponding to cervical nerve roots from C6 through C8 bilaterally.(ABSTRACT TRUNCATED AT 250 WORDS)

Cervical Vertebrae↗
PubMed1992

[A case of malignant rheumatoid arthritis with corticosteroid-reactive subacute myelopathy and multiple peripheral neuropathy].

We reported a 64-year-old man who had malignant rheumatoid arthritis (MRA) and developed subacute myelopathy and peripheral neuropathy. He had suffered from seropositive rheumatoid arthritis for 4 years, and developed weakness of four limbs, dysuria and constipation two months before the admission. Neurological examination revealed the diffuse muscle wasting and weakness in four limbs. Deep tendon reflexes were hyperactive in four limbs, but not in jaw jerk. Babinski sign was positive bilaterally. Deep sensation was decreased in four limbs and superficial sensation was decreased below the neck. Dysuria and constipation were noted, but anal and bulbocavernosus reflexes were present. On laboratory examination, RF and RAHA increased markedly. Serum complements decreased and immune complexes were positive. Nerve conduction study demonstrated multiple entrapment neuropathy in addition to mononeuritis multiplex. Histological examination of the biopsied sural nerve disclosed the obliterating endarteritis in the epineurium, and marked decrease in number of myelinated fibers. No compressive lesions were seen in the spinal canal by spine X-ray and MRI. Assuming that inflammatory process induced cervical myelopathy, corticosteroid therapy (predonisolone 60 mg/day) was administered and alleviated neurological symptoms, in accordance with the improvement of serological abnormalities. Therefore, an inflammatory process associated with MRA was supposed to damage the spinal cord as well as peripheral nerves in the present case.

Acute Disease↗
PubMed1992

[An autopsy case of spinal subdural abscess in the aged--comparative study with neuroradiological findings].

An 82-year-old woman without previous medical problem noticed vague back pain on December 31, 1989, and was admitted to a hospital because she developed a fever, a rapidly progressive weakness followed by anesthesia of the lower extremities and sphincter disturbance. On myelography and myelo-CT, the spinal cord appeared to be displaced by an extramedullary mass which partially blocked the subdural space at the level of T-9 to L-1. When transferred to our hospital on January 8, 1990, she was febrile and complaining of headache with meningeal signs. Percussion tenderness was present at T-8 to L-1 spinal spinous process. Neurological examination revealed that the patient had mild consciousness clouding, total paraplegia in the legs, sensory disturbance of a partial degree at L-1 to L-3 and totally below L-3, brisk but equal tendon reflexes in the upper extremities, areflexia in the legs with positive bilateral Babinski signs and sphincter disturbance. Otherwise she was neurologically unremarkable. Acute inflammatory reactions were prominent among the laboratory findings on admission. A lumbar tap yielded purulent fluid with more than 170,000 cells/mm3, 5,000 mg/dl of protein, 44 mg/dl of glucose and culture of the fluid isolated Escherichia coli. T1-weighted sagittal MRI disclosed an ill defined mass which showed the same or locally higher with gadopentetate dimeglumine (Gd-DTPA) signal intensity as soft tissue, compressing the spinal cord anteriorly from T-7 to L-3. The lesion was noticed to have a more extensive rostral-caudal extent than was inferred from myelography and myelo-CT.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1992

[Polyneuropathy in hyperthyroidism--a clinical neurophysiologic study].

In this prospective study, 27 patients with hyperthyroidism were evaluated neurophysiologically. There were 24 women and 3 men: the mean age was 56.4 years (range 21 to 84 years). Neurologic complaints of the patients were muscle weakness (59.3%), muscle cramps (18.5%) and sensory symptoms (11.1%). Tendon reflexes were increased in 18.5% and decreased in 14.8%, respectively. While the motor nerve conduction velocities (NCV) of the tibial and the peroneal nerve revealed normal results in the majority of patients, there were pathological findings of the sensory NCV of the sural nerve in 29.6% of patients. In another 22.2%, borderline findings were obtained. Six patients presented myopathic changings in electromyography of the m.vastus lateralis. Neither neuropathic nor myopathic findings correlated with the serum levels of TT3, TT4 or the T4/TBG-quotient. A polyneuropathy in hyperthyroidism seems not to be uncommon and is probably caused by hypermetabolism in thyroid hyperfunction.

Adult↗
PubMed1992

[Anomalous course of a lipomeningocele].

A 9 months old male with a lipomeningocele developed progressive flaccid paraparesis with loss of deep tendon reflexes and sensation to pink prick on the lower extremities. The clinical picture was secondary to a tethered spinal cord syndrome associated to the lipomeningocele. Surgical untethering of the spinal cord was followed by clinical recovery over a 3 months period.

Adipose Tissue↗
PubMed1992

[Two familial cases with exertion-induced heat stroke--relationship to malignant hyperthermia].

Two patients in a family of exertion-induced heat stroke were reported. Case 1: A 23-year-old male, paternal cousin of case 2, was admitted to our hospital because of loss of consciousness during running under a burning sun. On physical and neurological examinations, he was deeply comatose with high fever, tachycardia, and increased deep tendon reflexes. Laboratory findings disclosed rhabdomyolysis, acute renal failure, disseminated intravascular coagulation, liver injury, and brain edema. He recovered after intensive cooling, some antibiotics, glycerol and sodium dantrolene administration. Case 2: A 19-year-old male experienced loss of consciousness and high fever during playing soccer at 15 years of age, and was admitted to a hospital. On admission, he had high fever of 38.7 degrees C, and increased serum CK level. He recovered two weeks after admission. He was readmitted to our hospital to evaluate the predisposition for malignant hyperthermia. His physical and neurological examinations showed no abnormalities. Routine laboratory findings were within normal limits. Muscle biopsy findings of cases 1 and 2 were mildly increased number of fibers with centrally placed nuclei. Caffeine test on skinned muscle fibers from the biopsies showed normal response in both type 1 and 2 fibers. The present patients were diagnosed as having exertion-induced heat stroke, but with no increased muscle fiber sensitivity to caffeine, suggesting that the pathomechanism differs from that of malignant hyperthermia induced by malfunction of sarcoplasmic reticulum.

Adult↗
PubMed1992

[Varicella-zoster virus-associated spinal myoclonus without skin lesions].

A 50-year-old woman was admitted to our hospital because of abnormal involuntary movement of upper abdomen. Three months before admission, she had suffered from left lateral chest pain without skin lesions for one week. The neurological examination on admission revealed myoclonus of upper abdomen, and hyperalgesia and thermohyperesthesia from T4 to T9. There was no weakness, the tendon reflexes were symmetrical and the plantar responses were flexor. The surface EMG disclosed the symmetrical, synchronous contractions of m. rectus abdominis and m. obliques externus abdominis. This spinal myoclonus reduced during sleep. The EEG, CT and MRI showed no abnormalities. Serum varicella-zoster virus (VZV) titers increased significantly on follow-up examinations. Clonazepam, 1.5 mg daily was effective in this patient. The myoclonus spontaneously disappeared without clonazepam in six weeks after onset, and at the same time the sensory disturbance also improved. From the neurological findings and clinical course, we consider this spinal myoclonus was probably elicited by involvement of the inhibitory interneurons of the dorsal horns, due to immune response to latent VZV infection but not to direct neuronal destruction by VZV. Spinal myoclonus should be recognized as the spectrum of neurological disease associated with VZV even in the absence of skin lesions.

Female↗
PubMed1992

[A case of giant pigmented nevus with multiple meningiomas].

A 36-year-old female had a giant congenital pigmented nevus on her anterior trunk. She complained of muscle weakness of the right arm and leg in August 1988, and she was admitted to our hospital to take medical examinations in September 1988. Neurological examination revealed right hemiparesis and exaggerated deep tendon reflexes. Three small falx meningiomas were shown on CT scans and MR images, but they did not appear to be causes of her symptoms. CT-myelography and MR images revealed an intradural extramedullary tumor spreading from the foramen magnum to C2. Oncotomy and C1 laminectomy were performed. Histological finding was compatible with transitional meningioma. Neurological symptoms markedly improved after operation. This patient is considered as a case of neurocutaneous syndrome with central nervous system tumors. Considering that both giant pigmented nevus and meningioma originate from neural crest, they appear to be closely related each other. Such a combination of giant pigmented nevus and meningioma has not yet been reported.

Adult↗
PubMed1992

[Acute lymphoblastic leukemia with extensive demyelinated lesion of the brain stem during complete remission].

A case of acute lymphoblastic leukemia (ALL) which showed extensive demyelinated lesion of the brain stem during complete remission is presented. A 13 year-old girl who was diagnosed as ALL in February, 1987 was treated according to the TCCSG L84-11 protocol, which induced complete remission in June, 1987. Her condition had been stable until April, 1988 when she abruptly complained of gait disturbance, vertigo and anorexia. She was subsequently admitted to our hospital. At the time of admission, she had ataxic gait, horizontal nystagmus towards right at dextroversion, bilateral exaggerated patellar tendon reflex, emotional incontinence, urinary incontinence and left 6th and 7th nerve palsy. In the middle of May, right spastic hemipalesia and hypesthesia became apparent. Left caudal pontine-basal lesion was suspected and was confirmed by MRI. Her synptoms progressed. Five months after admission, suffered repeated central apnea and died. Autopsy disclosed extensive cervical spinal cord. Cerebrum and cerebellum were intact. No evident findings suggesting the etiology were obtained. Whole skull radiation, intrathecal methotrexate, cytosine arabinoside and hydrocortisone might have contributed to the development of the demyelinated lesion.

Adolescent↗
PubMed1964

DIABETIC NEUROARTHROPATHY: REPORT OF FOUR CASES.

Diabetic neuroarthropathy was observed in four patients; these are the first cases of this nature reported in the Canadian medical literature. The criteria for this diagnosis included: (1) long-standing diabetes; (2) arthropathy, most frequently involving the foot, which shows deformity, shortening and ulceration without evidence of infection or peripheral circulatory failure; (3) abolition or diminution of pain on weight-bearing; (4) diabetic peripheral neuropathy with impaired sense of position or vibration and weak or absent deep tendon reflexes. Radiographic findings were similar to those in patients with Charcot's arthropathy from any cause.Tabes dorsalis, leprosy, syringomyelia, myelodysplasia and the arthropathies of corticosteroid therapy were ruled out in these cases. In addition to conventional medical therapy the patients were treated by means of walking-casts for several months.Diabetic neuroarthropathy is probably more common than the medical literature would indicate. Diminished sensation in the lower limbs in diabetics of long standing appears to be the major factor contributing to this disorder.

Arthropathy, Neurogenic↗
PubMed1992

[A case of progressive supranuclear palsy dramatically improved with L-threo-3,4-dihydroxyphenylserine].

We report a 67-year-old female with progressive supranuclear palsy (PSP) who dramatically improved when given L-threo-3,4-dihydroxyphenylserine (L-DOPS). This patient developed dysarthria, lack of facial expression, and slowness at age 64. She was admitted to a local hospital, diagnosed as having parkinsonism and treated with antiparkinsonian drugs. Despite this treatment, she had difficulty in turning over in bed and standing up from a seat, and began to fall backward at age 65. One year later, she had trouble in walking due to frequent falls and became bedridden. The patient was admitted to our hospital in July 1991 under treatment with 20 mg/200 mg of carbidopa/L-dopa and 4 mg of trihexyphenydyl hydrochloride per day. Neurological examination revealed masked face, pseudobulbar palsy, and dystonic rigidity of the neck and upper trunk. Eye movements were normal except for impaired vertical saccades and convergence inability. Deep tendon reflexes were generally brisk and the plantar responses were flexor bilaterally. Tests of pulsion showed that her postural reflex was markedly disturbed, especially in retropulsion. Her gait showed severe unsteadiness. Neuropsychological tests showed intellectual impairment, frontal lobe dysfunction, and memory disturbance. Computed tomography showed an atrophic midbrain with prominent enlargement of ambient and quadrigeminal plate cisterns. Single photon emission computed tomography (SPECT) using 123-I-isopropyl-iodoamphetamine demonstrated marked frontal hypoperfusion. L-DOPS was administered at a dose of 100 mg per day and gradually increased up to 600 mg per day over a period of five weeks, while carbidopa/L-dopa and trihexyphenidyl hydrochloride were continued as on admission.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1992

[Lambert-Eaton syndrome: clinical and electrophysiological study of 18 cases associated with lung cancer].

The clinical and electrophysiological data of 18 consecutive adult patients with paraneoplastic Lambert-Eaton myasthenic syndrome (LMES) have been reviewed. The cancer associated with LEMS was small-cell lung carcinoma (SCLC) in 15 cases and epidermoid lung carcinoma in 3 cases. The main clinical neurological features were proximal lower limb weakness (100%), depressed tendon reflexes (94%) and dryness of the mouth (66%). The results of repetitive nerve stimulation (RNS) were not statistically different in the paraneoplastic LEMS group and in a group of 6 LMS patients in whom no carcinoma had been detected. Low-amplitude compound muscle action potential (CMAP) was present in all cases; decremental response at low stimulation rates was present in 13/15 cases. An abnormal incremental response at high stimulation rates was observed in all cases. A close correlation between CMAP amplitude and clinical condition was found in 4 cases during the long-term follow-up. In one patient the RNS electrical pattern could be misinterpreted as myasthenia gravis in only one muscle tested. We underline the usefulness of a 50 Hz stimulation during 4 seconds to establish the diagnosis unequivocally, and that of post-exercise facilitation in routine detection among an SCLC population. Our results suggest that CAMP amplitude and RNS test could be used to evaluate the short-term improvement of LMS under treatment and, in some cases, for the long-term follow-up. The infraclinical axonal neuropathy detected in 8 patients probably was another associated autoimmune paraneoplastic complication.

Adult↗
PubMed2003

[A case of anaphylactoid shock occurring immediately after the initiation of second intravenous administration of high-dose immunoglobulin (IVIg) in a patient with Crow-Fukase syndrome].

We report a case of anaphylactoid shock occurring immediately after the initiation of second intravenous administration of high-dose immunoglobulin (IVIg) in a patient with Crow-Fukase syndrome. The patient was a 57-year-old woman, who was admitted to our hospital because of numbness and muscle weakness in the four extremities, difficulty in walking, and foot edema. On admission, her skin was dry and rough, and also showing scattered pigmentation, small hemangiomas, and hypertrichosis in both legs. She had distal dominant muscle weakness, more prominent in her legs, and was not able to walk. Deep tendon reflexes in her four extremities were markedly diminished or absent. She had a glove and stocking type of paresthesia, severe impairment of vibration, and absence of joint position sensation in her four extremities. On laboratory data, serum vascular endothelial growth factor (VEGF) was markedly elevated to 5,184 pg/ml (normal: below 220 pg/ml). Cerebrospinal fluid examination revealed cell counts of 2/microliter and protein level of 114 mg/dl. Abdominal echo showed marked hepatosplenomegaly. On peripheral nerve conduction study, both motor and sensory conduction velocity were undetectable in her legs. We diagnosed her condition as Crow-Fukase syndrome, and started IVIg of polyethyleneglycol-treated gamma-globulin (PEG-glob) at 400 mg/kg/day for 5 consecutive days for polyneuropathy. Since the first IVIg mildly improved muscle weakness, we tried the second IVIg of PEG-glob. However, immediately after the initiation of second IVIg of PEG-glob, she developed hypotention, dyspnea, cold sweating, cyanosis, and became lethargic. We immediately stopped IVIg and started first-aid treatment with epinephrine and corticosteroid for these symptoms. This treatment was successful and the patient fully recovered without any sequelae. Since serum IgE level remained unchanged and lymphocyte stimulation test (LST) was positive against the same rot number of PEG-glob, we diagnosed these symptoms as anaphylactoid shock. Based on the results of LST, we speculated that PEG-glob was the causative agent of anaphylactoid reaction. Anaphylactic or anaphylactoid reaction as adverse effects of IVIg is very rare, and to our knowledge, there are only 4 previous reports of anaphylactic or anaphylactoid reaction caused by IVIg. Therefore, we speculated that the prominent high level of serum VEGF in the present patient might play a significant contributory role in the development of anaphylactoid shock, since the vascular permeability of VEGF is 50,000 times stronger than that of histamine. We consider that it is necessary to carefully monitor IVIg of PEG-glob administration for polyneuropathy in patients with high level of serum VEGF, like Crow-Fukase syndrome.

Anaphylaxis↗
PubMed2003

[Adult cases of viral meningitis caused by echovirus type 13].

Adult cases of viral meningitis caused by echovirus type 13 (E13) were studied. E13 was isolated from 8 of 11 adult patients (73%) with viral meningitis between April and September 2002 in Fukui Prefecture. The mean age was 27.4 +/- 6.4 years (4 males and 4 females). The disease was prevalent among adults, especially younger adults as well as children. The symptoms and signs were as follows; headache (100%), fever (100%), nausea and/or vomiting (88%), Kernig's sign (88%), and increased deep tendon reflexes (50%). The average cell counts in cerebrospinal fluid (CSF) were 118 +/- 111/mm3. Of the 2 patients, polynuclear cells were dominant during the early phase of the disease. The prognosis was good. Since May 2002, the number of patients with viral meningitis caused by E13 has rapidly increased. Most of the reported patients were children. We should consider the possibility of E13 infection as a cause of adult viral meningitis.

Adolescent↗
PubMedDate not supplied

[Iatrogenic botulism: a complication to be taken into account in the treatment of child spasticity].

INTRODUCTION: During the last decades the use of botulinum toxin for management of muscular disorders and spasticity associated to cerebral palsy has become a widespread practice. CASE REPORT: A 6-years female suffering of cerebral palsy secondary to a partial agenesis of the corpus callosum who was receiving bolulinum toxin since October 2001. One week after the last dose (Dysport 46 U/kg/dose) she started high grade fever, malaise, food refusal, choking, constipation, eyelid ptosis, absence of deep tendon reflexes, and abundant mucous discharge. Such features were so progressively severe that ventilatory support became mandatory. After a previous dose five months before, she developed similar features but they were less severe and thought to be related to a respiratory infection. CONCLUSIONS: At the present, there are two forms of botulinum toxin commercially available: the British brand Dysport and the American brand Botox. Bio equivalences are 1 U Botox to 2 or 6 U Dysport. Dosing (U/kg per session) has been established as follows: 5 U for Botox, 35 U for Dysport. Safety limits are a wide range with a therapeutic toxic index rate of 1:10. Generalized side effects after diffusion to blood of locally injected botulinum toxin are rare.

Agenesis of Corpus Callosum↗
PubMed1992

[An autopsy case of chronic inflammatory demyelinating polyradiculoneuropathy with sever degeneration in the posterior column].

An autopsy case of chronic inflammatory demyelinating polyradiculoneuropathy was reported. It took a progressive course and terminated fatally in eight years. A 41-year-old man noticed motor disturbances when he tried to lift a bath pail and to write on July, 1978. Neurological examination revealed proximal dominant muscle atrophy, weakness of all extremities, and moderately diminished tendon reflex. Sensation was normal. The CSF showed albumin cytologic dissociations. Electromyogram showed neurogenic changes. Histological examination of biopsy specimen obtained from the anterior tibial muscle revealed severe neurogenic changes and showed axonal degeneration on the ventral tibial nerve. The treatment by corticosteroids was not effective, and the disease gradually progressed with repeated improvements and exacerbations. Three years after the onset, he showed vesicorectal dysfunctions. He died of respiratory failure on May, 1986. Neuropathological examination showed severe degeneration of middle root zones in the posterior columns, loss of myelinated fibers in Clarke's columns, demyelination and mild loss of axons accompanied by lymphocytic infiltration in the spinal roots, especially in the anterior roots. The histogram of cervical ventral root, ventral and dorsal roots of thoracic and lumbar regions revealed a decreased number of large myelinated fibers. A characteristic finding of this case was the dissociation of clinical features and neuropathological findings; the clinical features showed a typical motor neuropathy, but neuropathological examination showed severe degeneration on posterior columns of spinal cord like a sensory-ataxic neuropathy. Our observation suggest that the pathway which originates from posterior ganglion cells and runs into Clarke's columns passes through the middle root zones, since severe demyelination in Clarke's columns was observed.

Adult↗
PubMed2003

[Acute quadriplegia after diabetic ketoacidosis].

A 36-year-old female was admitted to the intensive care unit after resuscitation diagnosed with diabetic ketoacidotic coma, which was the first manifestation of her diabetes mellitus. It may have been provoked by pulmonary or gastrointestinal coinfection. Five days following admission the patient regained consciousness and homeostasis returned to normal. One week after the stabilization of her cardiopulmonary state, weaning from the respirator turned out to be unsuccessful: flaccid tetraparesis developed with rapid muscle atrophy and absence of deep tendon reflexes. The sensory system and cranial nerves remained intact. Electrophysiological studies and muscle biopsy showed serious acute illness myopathy with mild demyelination owing probably to the latent diabetes. The course of acute quadriplegia was fluctuating and correlated mainly with the activity of the systemic inflammatory response syndrome mechanisms. Myopathy might have been aggravated by using high-dose glucocorticoid therapy. The patient's general condition improved quickly as a result of full recovery from sepsis, discontinuation of glucocorticoids and normoglicaemia maintained by subcutan insulin substitution. Eight months after admission almost full neuromuscular restitution was achieved showing the reversibility of this grave illness.

Acute Disease↗
PubMedDate not supplied

Persistent elevated serum levels of intact parathyroid hormone after reoperation for primary hyperparathyroidism and after pamidronate therapy.

Primary hyperparathyroidism is a life-threatening rare disorder. It is seen as a result of neonatal primary hyperparathyroidism, familial hypocalciuric hypercalcemia, increased vitamin D levels and inactivation of calcium sensing receptor mutations. The clinical findings are hypotonia, bone demineralization, hypercalcemia and parathyroid hyperplasia. We present a six-month-old female patient, the first child of nonconsanguineous parents, who was referred for the investigation of failure to thrive, vomiting, constipation, fever, abdominal distention and hypotonia. Physical examination revealed weight under 3rd percentile, height 3rd-10th percentile, decreased subcutaneous fat, and distention of the abdomen. In neurological examination, hypotonia, motor-mental retardation, and active deep tendon reflexes were found. The biochemical values at the time of admission revealed primary hyperparathyroidism. Since hypercalcemia did not respond to calcitonin therapy and due to the mortality of hypercalcemia, parathyroidectomy was performed. Because hyperparathyroidism and hypercalcemia continued, angiography was done which revealed increased parathyroid hormone levels in the periphery of the innominate vein. Exploratory surgery followed, but hyperparathyroidism and hypercalcemia persisted after all of these procedures. Calcium-sensing receptor mutations and supernumerary gland were considered. Because hypercalcemia persisted, pamidronate therapy was initiated on a monthly basis.

Anti-Inflammatory Agents↗