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PubMed1993

Prevalence and clinical correlates of cardiovascular autonomic and peripheral diabetic neuropathy in patients attending diabetes centers. The Diacan Multicenter Study Group.

The objective of the study was to evaluate the prevalence of and the factors associated with cardiovascular autonomic diabetic neuropathy (CADN) and peripheral neuropathy in patients attending clinical and outpatient diabetes centers. The design was a multicenter cross section study with random selection of patients with Type 1 or Type 2 diabetes from seventeen German, three Swiss, and two Austrian inpatient and outpatient diabetes centers. A total of 1,642 patients were recruited, 1,171 of whom (Type 1: n = 647, age: 11-69 years; Type 2: n = 524, age: 16-72 years) were studied. Measurements and results. The following six autonomic function tests based on heart rate variation were used for the diagnosis of CADN: coefficient of variation and power spectrum in the low- and mid-frequency bands at rest, mean circular resultant during deep breathing, Valsalva ratio, and max/min 30:15 ratio to standing. The age-dependent lower limit of the normal range in these tests had previously been defined at the 2.3 centile in 120 healthy subjects. Definite CADN defined by the strict criterion of abnormal results in > or = 3 of these 6 tests was detected in 16.8% of the Type 1 and 22.1% of the Type 2 diabetic patients (p < 0.05). The corresponding rates of borderline CADN defined as the presence of 2 abnormalities were 8.5% and 12.2%, respectively (p < 0.05). Peripheral neuropathy defined as the presence of > or = 2 abnormalities among 3 criteria (neuropathic symptoms, absent tendon reflexes, and abnormal malleolar vibration perception threshold) was observed in 17.1% of Type 1 and 34.8% of Type 2 diabetic patients (p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMedDate not supplied

[Lowe syndrome: report of one case].

The Lowe syndrome, or oculocerebrorenal syndrome, is a rare X-linked recessive hereditary disease which typically involves three major systems including ocular defects (congenital cataracts, glaucoma, searching nystagmus), central nervous system defects (generalized hypotonia with decreased or absent deep tendon reflex and severe mental retardation), and renal dysfunction (progressive renal tubular dysfunction with acidosis and hyperaminoaciduria). Less than 200 cases have been reported in the English literatures since 1952. This article presents the first case of Lowe syndrome in Taiwan. Patient was a newborn who was born with congenital cataracts, glaucoma, generalized hypotonia with areflexia. In following laboratory studies showed early manifestations of renal tubular dysfunction with metabolic acidosis, proteinuria, glycosuria, phosphaturia and generalized hyperaminoaciduria (19 types). CT of brain showed an arachnoid cyst about 4.5 x 5 cm in size below the cerebellar tentorium. Large amount of copper, about 20-30 times above normal range, was detected in the urine. To our knowledge, Lowe syndrome associated with hypercupriuria and arachnoid cyst has not been reported in the past. Whether hypercupriuria is a part of the entity of this disease or prodromal stage of Wilson's disease is obscure. Further investigation and long-term observation are necessary to draw any conclusion.

Arachnoid Cysts↗
PubMed1993

[An autopsied Japanese case of hereditary olivo-ponto-cerebellar atrophy compatible with the original one of Menzel's report (1891)].

We report a patient whose clinicopathological findings are compatible with those of the case reported by Menzel in 1891. This case was briefly reported by Kinoshita et al in 1967 as hereditary ataxia of Menzel type. But the concept of this disease has been confused, especially in the early investigations for the hereditary olivo-ponto-cerebellar atrophy (OPCA) in Japan. The Kinoshita's patient should be considered as the first Japanese case whose findings are identical with Menzel's report. This report represents a precise study of the case reported by Kinoshita et al. The patient was a 42-year-old Japanese woman. Her mother and one of her brothers suffered from the same disease. She began to experience progressive ataxia at the age of 30. At age 42, she was admitted to another hospital because of inability to walk and mental deterioration. Neurological examination revealed cerebellar ataxia in the extremities and trunk, childish personality change, dementia, diminished deep tendon reflexes with extensor plantar response bilaterally, slowness and hypokinesia in the movement, generalized muscular atrophy, and sensory disturbance prominent in deep sensory. She had no involuntary movement and dysautonomia. She had no retinal degeneration, nystagmus, nor progressive nuclear oculomotor palsy. She died of pneumonia. Neuropathological findings revealed brain weight of 850g.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

[Familial juvenile parkinsonism with dementia and autonomic failure--a case report].

A case of familial juvenile parkinsonism with dementia, orthostatic hypotension, neurogenic bladder and constipation was reported. He had been in a good health until the age of 28 when a finger tremor occurred on effort to hold hands in a definite position, and disturbances in gait and speech were noted. These symptoms were relieved by levodopa treatment followed by dyskinesia and motor fluctuations. Three years later, he complained of faintness, constipation and urinary frequency. The neurological examination revealed mentally sound male with masked face, tremor and rigidity in his extremities, and short step gait with lateropulsion. Urodynamic study showed uninhibited bladder. In the following years, orthostatic hypotension, dysuria and urinary retention developed gradually. He became mentally loose and was unable to take medicines appropriately. When in the Nishiojiya Byoin National Sanatorium, he tried to snake out the hospital many times. His parents and a brother suffered from Parkinson's disease and juvenile parkinsonism, respectively, suggesting an autosomal dominant inheritance. On admission to our hospital, he was apathetic. He had masked face, bilateral postural tremor, frozen gait and dyskinesia in the right lower extremity. Little bradykinesia or rigidity was noted. His muscle tone and deep tendon reflexes were decreased but neither muscular wasting, weakness, ataxia nor sensory disturbance was observed. Laboratory data including ceruloplasmin, copper, dopamine-beta-hydroxylase and lysosomal enzyme activities were normal except for mild anemia. A cranial CT scan revealed mild cortical atrophy in the frontal and temporal lobes, but nerve conduction study and cortical evoked potentials showed no abnormality. While in the hospital, his mental functions deteriorated to the state of dementia and orthostatic hypotension became apparent.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

[Guillain-Barré syndrome and pregnancy].

Guillain-Barré syndrome is a rare occurrence in pregnant women. We describe the case of a 21-year old woman, seen at "Nuevo Hospital Civil de Guadalajara" with a term pregnancy, who presented with limbs weakness and paresthesias, drowsiness and malaise. Her vital signs were normal but she was quadriparetic, there was muscular atrophy in the extremities and deep tendon reflexes were decreased. Spinal fluid analysis revealed a protein of 71.2 mg/dl, glucosa 48 mg/dl and no white cells and both Gram stain and routine cultures were negative. EMG studies reported poliradiculoneuritis; a C-section was done, and both the mother and a newborn girl did very well. Guillain-Barré syndrome should be suspected in similar cases in order to offer prompt intervention.

Adult↗
PubMed1993

[A case of X-linked recessive bulbospinal muscular atrophy with demyelinating neuropathy and hypertrophy of the calves].

We report a 53-year-old man of X-BSMA with neuropathy. The patient developed slowly progressive muscular weakness and wasting over a 2-year period with an accompanying numbness in the finger tip. He can run normally but not so fast. When he was aged 52-year old, difficulty in running progressed. General physical examination revealed nothing particular except for hypertension and gynecomastia. He showed muscular weakness and atrophy in the tongue, shoulder girdle, and upper and lower limbs. Calf muscle hypertrophies were prominent on both sides. The tendon reflexes were absent. Slight sensory impairment for vibration and pin-prick was present distally in all limbs. Autonomic nerve dysfunction was not observed. Hyperglycemia, elevated HbA1c and elevated serum CK (1,242 IU/l) were seen. The computed tomographic analyses on skeletal muscle showed hypertrophic changes in the calf muscles with a few fatty infiltrations. Electromyography showed a systemic neurogenic pattern. Motor nerve conduction velocities were slightly delayed in the lower limits. Sensory nerve action potentials were not elicited in all nerves tested. Sural nerve biopsy disclosed marked reduction of myelinated fibres for that of large diameter with thin myelin. Teased fibre studies showed a definite increase in the incidence of fibres with segmental demyelination and remyelination. In electron microscopic examination, typical or atypical onion bulb formation was observed on individual fibres. Axonal changes were minimum. We believe that segmental demyelination observed in this patient is not secondary to axonal damage. We, also, investigated AR gene abnormality by polymerase chain reaction (PCR) in this patient.(ABSTRACT TRUNCATED AT 250 WORDS)

Demyelinating Diseases↗
PubMed1993

[A case of hereditary motor and sensory neuropathy type I with optic atrophy, neural deafness and pyramidal tract signs].

A case of hereditary motor and sensory neuropathy (HMSN) type I with optic atrophy, neural deafness and pyramidal tract signs was described. The patient was a 53-year-old man who had suffered from difficulty in walking, decreased visual acuity since age 16 years. These symptoms were slowly progressive. At the age of 37, he was pointed out optic atrophy, positive pyramidal tract signs. Distal muscle weakness with atrophy of four limbs was prominent at the age of 50. Since then, he noticed progressive hearing loss with blindness. His elder sister was diagnosed Charcot-Marie-Tooth disease. On neurological examination, he showed to have optic atrophy without retinitis pigmentosa and neural deafness. Also he showed mild degree of muscle weakness and atrophy in four limbs, severe in the distal part of lower limbs. Deep tendon reflexes were absent in all limbs with right Babinski sign. Superficial sensation was decreased slightly in the distal parts of four limbs. Deep sensation was markedly decreased in the leg. There were no cerebellar signs. Audiometric examination revealed bilateral neural hearing loss. There were no findings of spinal cord compression on spinal MRI. On the nerve conduction studies, sensory nerve action potential was not elicited in all nerves tested. Motor nerve conduction velocity of the right median was 41.1 M/sec, also ulnar nerve 44.7 M/sec, but M-wave was not elicited with the electrical stimulation of other tested nerves. On sural nerve biopsy, the density of myelinated fibers was severely decreased. Well-myelinated axon surrounded by onion bulb formation was observed in electron microscopic examination.(ABSTRACT TRUNCATED AT 250 WORDS)

Charcot-Marie-Tooth Disease↗
PubMed1993

[A case of Hallervorden-Spatz syndrome with marked atrophy of the brainstem and cerebellum].

We report a 20-year-old female with Hallervorden-Spatz syndrome (HSS). This patient is the product of consanguineous parents. She developed genu valgum, tendency to fall and mental deterioration at the age of 6, decrease of the number of spoken words at the age of 14, dysarthria, unsteady gait, postural tremor of the upper extremities, dystonic posture of hands and double incontinence at the age of 16. Her disease progressed slowly. Neurological examination on admission revealed severe mental retardation, optic atrophy, forced grasping, hyperactive tendon reflexes in the upper extremities and bilateral Babinski sign. An extensive laboratory investigation including the leukocyte lysosomal enzymes, serum amino acid analyses, copper studies and ceruloplasmin were almost within normal limits. MRI, T2 weighted images, showed markedly decreased signal intensity in the globus pallidus but substantia nigra and increased signal intensity in diffuse cerebral white matter. T1 weighted images showed marked atrophy of the brainstem and cerebellum. She met the diagnostic criteria for HSS by Swaiman; we diagnosed her as HSS group II. HSS is characterized by the presence of many spheroids in the central nervous system which is similar to neuroaxonal dystrophy (ND). However, clinical and pathological differences exist between HSS and ND, the precise classification of the two conditions has remained controversial. Although there are many reported cases in which both conditions overlap, this is the first reported case that simultaneously demonstrates increased iron deposition in the globus pallidus, marked atrophy of the brainstem and cerebellum and typical clinical course compatible with HSS.

Adult↗
PubMed1993

[A case of diagnostic dyspraxia without ideomotor apraxia by callosal lesion].

A case of diagnostic dyspraxia was reported. A 57-year-old right handed male had been suffering from the lack of cooperation between his right and left hands for six months. Except for decreased deep tendon reflexes in all extremities, there were no abnormal findings on neurological examination. On neuropsychological examination, he was attentive, well orientated and his spontaneous speech, comprehension, naming, repetition and reading were intact. There was peculiar dissociative behavior between his right and left hands. For instance, he put a cigarette or coin in the pocket with his right hand then his left hand took out and replaced them, and he buttoned his shirts with his right hand but then unbuttoned with his left hand. These left hand oppositional behavior to his right hand were triggered by voluntary activities of his right hand. Left unilateral agraphia was also revealed but ideomotor apraxia, compulsive manipulation of tools and grasp reflex were not demonstrated. T1-weighted MRI demonstrated irregular low signal intensity areas extending from the genu to the body of the corpus callosum. No definite lesion was detected in the medial aspect of the frontal lobe. Only small numbers of diagnostic dyspraxia have been reported and such cases without ideomotor apraxia or medial frontal lesion are even rare. MRI is very useful for detecting the lesion of the corpus callosum.

Apraxias↗
PubMed1993

[A case of acute polyradiculoneuropathy following measles infection].

A 39-year-old man was admitted to our hospital because of diplopia, dysphagia, tetraparesis and urinary incontinence which developed six days after fever and general cutaneous rash had appeared. On neurological examination, total ophthalmoplegia, blepharoptosis, facial nerve palsy, bulbar palsy, and tetraparesis were observed, and the deep tendon reflexes were hypoactive or absent. The cerebrospinal fluid (CSF) showed albumin-cytological dissociation. serial complement fixation tests and enzyme-linked immunosorbent assays showed an elevation of antibody titers to measles virus in sera and CSF including serum IgM antibody. On the basis of findings, we diagnosed him as acute polyradiculoneuropathy following measles infection. After 3 sessions of immunoadsorption plasmapheresis his symptoms improved promptly. Marked improvement by immunoadsorption plasmapheresis suggested that immune-mediated mechanisms were involved in the pathogenesis of acute polyradiculoneuropathy following measles infection.

Acute Disease↗
PubMed1993

[A case of carcinomatous neuropathy with degeneration of posterior spinal column on MRI].

The patient was a 55-year-old man. He was well until eleven months earlier, when he noticed the onset of numbness in his right fingers. Over the next three months, the numbness spread up the right arm and involved the right leg, left arm and left leg in succession. Six months before admission, sensory impairment of the trunk appeared progressively. Mild diffuse muscle weakness occurred gradually. Swelling of the right lateral cervical lymph node was found just before admission. On neurological examination, sensory disturbance involving all modalities of sensation was recognized in the extremities and trunk. The sensory findings were asymmetric and predominant at the lower extremities and distal parts. A positive Romberg's sign and poor coordination was recognized. All the deep tendon reflexes were absent without pathological reflexes. Motor weakness, which was less severe than sensory findings, was present. There was no sphincter disturbance nor orthostatic hypotension. Routine laboratory findings were within normal limits. The protein level of cerebrospinal fluid was slightly increased. The electrophysiological studies and histological evaluation of the biopsied peroneal muscle and sural nerve showed degeneration and reduction of large myelinated fibers of sensory nerves with minimal motor nerve changes. Histological study also revealed the increase of regenerating fibers. Squamous cell carcinoma of epipharynx with metastasis of neck lymph nodes was found. Radiotherapy without chemotherapy resulted in a complete tumor remission and probably suppressed the progression of neurological disturbances. After two years from the onset, diffuse high intensity area was noted in the posterior spinal column on T2 weighted MRI.(ABSTRACT TRUNCATED AT 250 WORDS)

Carcinoma, Squamous Cell↗
PubMed1993

[Double meningoencephalitis with herpes simplex virus and rubella virus].

A 47-year-old man suffered from a headache, fever and memory disturbance. He was admitted to Morimoto Hospital. Neurological examination revealed disturbance of memory of recent events. Cranial nerves were normal. Muscle strength of the extremities was normal, except for Barré's sign of the right upper extremity. Deep tendon reflexes were exaggerated bilaterally, and extensor plantar response of the left side was elicited. Sensory examination showed no abnormality. Cerebellar sign was not recognized. Meningeal sign was slightly but clearly showed. CT scan demonstrated brain swelling at the right insular cortex region followed by severe hydrocephalus with dilatation of the lateral and the third ventricles. Cerebrospinal fluid showed high CSF pressure (250 mmH2O), pleocytosis (C.C. 359/mm3) and elevated protein level (213 mg/dl). Virological examination revealed herpes simplex virus (HSV) (CF) 32x, HSV-1 IgG (EIA) 4,050X, rubella virus IgE (EIA) 6,060X, cytomegalovirus (CMV) IgG (EIA) 1,130X in serum and HSV (CF) 1X, HSV-1 IGg (EIA) 1,430X, rubella virus IgG (EIA) 1,480X, CMV IgG (EIA) 587X in CSF. The ratio of serum/CSF of HSV and rubella virus titers by EIA methods were 2.83 and 4.10, respectively. He was treated by acyclovir 1,000 mg/day and gamma globulin, but his condition get worse acutely and died at 15th hospital days. This case was considered as a meningoencephalitis caused by simultaneous HSV and rubella virus infection.

Antibodies, Viral↗
PubMed1993

[A case of paraneoplastic autonomic and sensorimotor neuropathy with dysfunction in the afferent limb of baroreflex arc].

A 65-year-old man visited our hospital with complaints of tingling sensation in the distal parts of his extremities and dysuria, which first appeared 2 months before admission. He had no abnormal findings on physical examination. Neurological examination revealed sensory impairment of glove and stocking type, mild motor weakness and muscular atrophy in the proximal parts of arms and legs, and absent tendon reflexes in knees and ankles. Fasciculation was observed on his shoulders and upper extremities, and myokymia on the abdominal wall and bilateral calves. He had hyponatremia, which was proved to be caused by SIADH. Anti-acetylcholine receptor antibody, anti-GM1 ganglioside antibody and anti-galactocerebroside antibody were detected in the serum. Chest X-ray showed mass shadows in the mediastinum, which were confirmed as malignant thymoma by needle biopsy. Orthostatic hypotension, neurogenic bladder and anhidrosis were observed by the autonomic function tests. Lesions responsible for orthostatic hypotension and SIADH were suspected in the afferent fibers from baroreceptors, since an reactive increase of plasma arginine vasopressin to orthostatic hypotension was blunted and reflex hypertension in the cold pressor test was well-preserved, while overshoot in Valsalva's maneuver was absent. It is important that afferent baroreceptor dysfunction may be associated with paraneoplastic neurological syndrome, since lesions in acute autonomic neuropathy are usually in the efferent fibers.

Afferent Pathways↗
PubMed1993

[A case of multiple sclerosis associated with chronic inflammatory demyelinating polyradiculoneuropathy].

We report a 19-year-old girl with multiple sclerosis (MS) who had chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). At the age of 9 (1981), she was diagnosed as having Devic disease, including optic neuritis and transverse myelitis. For two years after the onset of the disease, she suffered from three relapses of MS and was treated with prednisone. At the age of 11, she noticed muscle weakness and sensory disturbance of four limbs. On examination, all tendon reflexes were absent, CSF protein was elevated, and motor nerve conduction velocity of the ulnar nerves was markedly slowed. Sural nerve biopsy showed decreased density of myelinated fibers and de-re-myelinated fibers with onion-bulb formations. Between 11 and 19 years, she had a number of episodes of the central nervous system (CNS) and peripheral nervous system (PNS) deficits with partial or complete recovery by oral administration of prednisone. The clinical course and laboratory data are consistent with MS associated with CIDP. Such our case of MS with CIDP in childhood is very rare. Patients with MS and CIDP may represent a subpopulation who had a common pathogenetic factor for both CNS and PNS demyelination.

Adult↗
PubMed1993

Lumbar spinal stenosis: clinical/radiologic therapeutic evaluation in 145 patients. Conservative treatment or surgical intervention?

In this prospective study, 145 patients with lumbar spinal stenosis were evaluated for clinical signs and radiologic findings and conservative treatment results. Clinical parameters such as pain on motion, lumbar range of motion, straight leg raising test, deep tendon reflexes, dermatomal sensations, motor functions and neurogenic claudication distances were assessed at admission and were compared after a conservative treatment program was completed. A conservative treatment program consisted of physical therapy (infrared heating, ultrasonic diathermy and active lumbar exercises) and salmon calcitonin. Pain on motion (100%), restriction of extension (77%), limited straight leg raising test (23%), neurogenic claudication (100%), dermatomal sensory impairment (47%), motor deficit (29%), and reflex deficit (40%) were observed in the patients. All aforementioned disturbances except reflex deficits improved by the conservative treatment and results were statistically significant. The authors conclude that this conservative treatment should be the treatment of choice in elderly patients and in those patients without clinical surgical indications.

Calcitonin↗
PubMed1979

Prenatal methylmercury poisoning. Clinical observations over five years.

Thirty-two infants prenatally exposed to methylmercury and their mothers were examined over a five-year period after the Iraqi methylmercury epidemic. Severity of poisoning in mothers was related to the peak mercury concentration in their hair and in the infants to the maximum concentration in maternal hair during pregnancy. In nine cases of cerebral palsy, methylmercury exposure occurred only during the last trimester. All infants except three (two were orphaned soon after birth and one was bottle-fed) were exposed postnatally via suckling. Whereas the mother's symptoms usually improved, the damage to the fetal nervous system appears to be permanent. Milder cases previously not identified in other studies are reported. The syndrome consists of varying degrees of developmental retardation in addition to exaggerated tendon reflexes and the pathologic extensor plantar reflex (minimal brain damage syndrome).

Abnormalities, Drug-Induced↗
PubMed1993

[Creutzfeldt-Jakob disease transmitted by cadaveric dural graft: a case report].

We report a case of Creutzfeldt-Jakob disease in a 38-year-old man, transmitted by a cadaveric dural graft. In August 1985, he underwent cranial nerve decompression for hemifacial spasm and received a cadaveric dural graft for dural closure. He had been well until he began to complain of blurred vision and headache in May, 1990. He developed dementia, myoclonus and urinary incontinence over the subsequent 3 months. He was admitted to our hospital in August, 1990. On admission, he was somnolent and showed gait disturbance, myoclonus in extremities and elevated deep tendon reflexes symmetrically. The results of analysis of blood, urinary and cerebrospinal fluid were normal. The initial computed tomography (CT) and magnetic resonance imaging detected no abnormality. Electroencephalography showed typical periodic synchronous discharge (PSD). There was progressive worsening of his neurological symptoms, and this developed into mutism in September, 1990. CT, 11 months after clinical onset, showed marked enlargement of the ventricles and the sulci. In view of his rapid worsening clinical course, PSD findings on electroencephalography, and delayed progressive changes of CT findings, the diagnosis of CJD disease was made. The cadaveric dural graft was suspected as the cause of the patient's condition. Since Thadani et al reported the first case of CJD transmitted by cadaveric dural graft in 1988, 3 other cases have been reported. This is most likely the 5th reported case of Creutzfeldt-Jakob disease transmitted by cadaveric dural graft.

Adult↗
PubMed1993

[A case with severe neurological involvement due to vitamin B1 deficiency associated with megaduodenum].

We reported a case of 4-year-old boy with multiple vitamin deficiencies, especially vitamin B1 deficiency. He had megaduodenum associated with membranous stenosis on upper jejunum. He showed recurrent vomiting at his infantile period, and recently intermittent neurological symptoms. When he was admitted to our hospital, he could not walk and showed masked face, absent deep tendon reflexes, horizontal and vertical nystagmus, proximally dominant muscle weakness and multiple vitamin deficiencies. Oral administration of small doses of vitamin B1 (20 mg/day) could make remarkable clinical improvements. At three weeks after the treatment he could walk and run. Before the admission he had febrile convulsions and showed transiently striatal low density on CT image. We concluded that his neurological symptoms were due to vitamin B1 deficiency associated with megaduodenum. When a patient with intestinal anomaly shows neurological symptoms, we should think of vitamin deficiency.

Child, Preschool↗