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PubMed1994

[Transcortical sensory aphasia in a patient with metastatic brain tumor in the left frontal lobe].

We reported a case of a 62-year-old right-handed woman who had transcortical sensory aphasia caused by a metastatic brain tumor in the left frontal lobe. She had mild right hemiparesis involving the face, without hyperactive tendon reflexes. She had neither sensory disturbance nor other cranial nerve deficits. Her spontaneous speech was fluent, and she sometimes had echolalia. Her object naming, word fluency, verbal comprehension and writing were severely disturbed. This contrasted with full preservation of repetition of phonemes and short sentences. Reading of words was preserved. CT scan revealed a subcortical lesion in the left superior frontal gyrus. Gd-enhanced MRI showed a ring-enhanced mass lesion in the frontal lobe outside of Broca's area. We thereby concluded that transcortical sensory aphasia may be caused by frontal lobe lesion independent of the perisylvian speech areas.

Adenocarcinoma, Papillary↗
PubMed1994

[Isolated oculomotor nerve palsy caused by mesencephalic hemorrhage].

A 62-year-old man with a history of diabetes mellitus, hypertension and liver damage has sudden diplopia on Nov. 4, 1992. Ocular movements of this right eye were normal, but his left eyelid was completely ptotic, and left pupil was dilated and nonreactive to light. In primary position, his left eye deviated outward, and could not move to any direction. He was diagnosed as having total oculomotor nerve palsy of the left side without any other neurological signs or symptoms; his consciousness level was alert and mental state was normal. The present case showed normal facial sensation, no facial palsy and no tongue deviation. Deep tendon reflexes were hypoactive bilaterally. Pyramidal tract sign, cerebellar sign, and gait disturbance were not observed. Superficial sensation of the extremity was normal. Brain CT scan revealed a small mesencephalic hemorrhage extending to the tegmentusm ventral to the cerebral aqueduct of the left side. Brain magnetic resonance imaging demonstrated a high-intensity area in the left oculomotor nucleus and its fascicles in the midbrain on T1- and T2-weighted image. The oculomotor nerve palsy of the left eye gradually improved, but mydriasis, adduction impairment and downward gaze palsy continued, and oculomotor nerve palsy of the left eye was compatible with so-called inferior branch palsy of the oculomotor nerve. Moreover, contralateral eye movements were normal except for mild upward gaze palsy. Oculomotor nerve palsy of this type was consistent with the syndrome of oculomotor nucleus described by Pierrot-Deseillingny in 1981. It was presumed that the superior rectus muscle is innervated by the contralateral oculomotor nerve nucleus in man as well as in animals.

Cerebral Hemorrhage↗
PubMed1995

[A boy with Emery-Dreifuss muscular dystrophy].

We reported a 12-year-old boy with Emery-Dreifuss muscular dystrophy (EMD). He was born after uncomplicated full term pregnancy and delivery. There was neither consanguinity nor a history of neuromuscular disorders or cardiac diseases in his family. He walked at 14 months. Toe walking was recognized at age 5 years. Examination at age 12 years showed the following. He could walk and climb stairs. There was no Gowers' sign. He had mild weakness of muscles except for face muscles. He had joint contractures at heels, elbows and knees. Deep tendon reflexes could not be elicited. Serum creatine kinase activity was significantly raised. Electromyography showed a myogenic pattern. Muscle biopsy from the left quadriceps showed mild dystrophic changes. 24 h Holter monitoring showed atrioventricular block with Wenckebach phenomenon. Prognosis in EMD is strongly connected with cardiac involvement. Therefore, we must follow up this case carefully for cardiac symptoms.

Biopsy↗
PubMed1994

[Isolated proximal muscular weakness disclosing myasthenic syndrome].

Three cases of chronic limb-girdle myasthenia gravis (one man and two women) are reported. The duration of the disease was three, five and 20 years respectively. None had oculobulbar weakness during this period nor fluctuating symptoms. The primary diagnosis was myopathy in two cases and myelopathy in the other one. In view of this diagnosis, several features were atypical: absence of marked wasting, preservation of tendon reflexes and normal serum creatine kinase activity. Finally, diagnosis of myasthenia gravis was established by the occurrence of a characteristic decremental muscular response to repetitive stimulation and by positive edrophonium test. It seems that the rate of positivity of acetylcholine receptor antibody is lower than in the common form of the disease. Two patients responded to acetylcholinesterase inhibitors and one to high-doses intravenous human immunoglobulins. These and previous cases described in the literature raise the problem of the definition of an unusual form of myasthenia gravis or of a new type of neuromuscular disease characterized by the presence of distinctive changes on muscular biopsies, specially tubular aggregates as in one of our cases. However, this unusual form of chronic limb-girdle weakness has to be recognized because treatments are effective in most cases.

Adult↗
PubMed1994

[Migrating radiculopathy--an unusual complication of systemic lupus erythematosus in an HTLV-1 carrier].

We reported a 54-year-old HTLV-I seropositive female patient with systemic lupus erythematosus (SLE), who developed migrating radiculopathy but without chronic progressive myelopathy. She occasionally noticed butterfly rash and photosensitivity of the skin as well as painful episodes in different joints for 10 years. She developed pins and needles sensation on her trunk a few days after she experienced lumbago with abrupt onset. Neurological examinations revealed normal muscular strength, exaggerated deep tendon reflexes without Babinski signs, and dysesthesia on her upper extremities and the trunk. The latter symptom showed a segmental distribution of spinal nerve roots. And during the course of the disease, it migrated in accord with a radicular pattern. This sensory disturbance was fairly responsive to corticosteroid treatment. The spinal tap yielded clear cerebrospinal fluid (CSF) which showed mononuclear pleocytosis (16/mm3) with predominance of CD8+ cytotoxic cells and a positive result for anti-HTLV-I antibody. A neurological status deteriorated in parallel with non-neurological symptoms as SLE, when the patient had discontinued corticosteroids in a tapering course by herself. We postulate that HTLV-I infection in this patient modulated original autoimmune reactions as SLE, which led to manifestation of migrating radiculopathy possibly due to autoimmunity against ganglion cells. This is, to our knowledge, the first report of migrating radiculopathy in an SLE patient associated with HTLV-I infection.

Carrier State↗
PubMed1994

Dural arteriovenous malformation with symmetrical calcification of the basal ganglia: a case report.

Dural arteriovenous malformations associated with symmetrical calcification of the basal ganglia are rare in children. This report concerns a 22-month-old female infant who was admitted with the problem of acute onset of status epilepticus. Physical examination revealed a grade II/VI heart systolic murmur over the left sternal border, and engorged scalp veins. Neurologically, left side hemiparesis, brisk deep tendon reflexes, bilateral presence of Babinski sign and ankle clonus were present. Brain computed tomography without contrast medium showed cortical atrophy and symmetrical calcification of the basal ganglia. Brain magnetic resonance imaging showed a signal-voided tortuous structure over the right parietal region. Cerebral angiography disclosed a dural arteriovenous malformation, located over the right parietal region, which had two major feeding arteries from the branch of the anterior cerebral artery and the parietal branch of the middle cerebral artery, and had direct venous drainage into the superior sagittal sinus. The patient received craniotomy with ligation of feeding arteries. She became seizure-free, and her neurological deficits improved gradually.

Basal Ganglia↗
PubMed1994

[Hepatitis B virus antibody positive spastic paraparesis].

We present here thirteen patients (5 men and 8 women, aged 31 to 73, mean 55 years) with spastic paraparesis who showed clinical features similar to those of HTLV-1 associated myelopathy without HTLV-1 antibody, but with positive antibody to hepatitis B virus (HBV). All of these patients showed slowly progressive difficulty in walking. Five patients had previous histories of blood transfusion, of these one with history of B hepatitis. Neurologically, muscle weakness, spasticity and exaggerated deep tendon reflexes in the lower extremities were common to all the patients. Seven patients showed Babinski's reflex. Disturbance of micturition was noted in 3 patients. None showed organic changes of the spine on magnetic resonance image (MRI). None was serologically positive for syphilis and had cryoglobulin and hypergammaglobulinemia. Elevated levels of the liver enzymes were noted in two patients. All patients were positive for hepatitis B surface antibody (HBs-Ab) (EIA) but negative for hepatitis B surface antigen (HBs-Ag) (EIA). Five patients were seropositive for hepatitis C virus (HCV) (PHA). In 3 of them, reverse transcriptase polymerase chain reaction was performed but failed to detect HCV-RNA. All patients underwent spinal tap, and showed normal cell count and protein concentration in their cerebrospinal fluid (CSF). Atypical cells were not observed in all the patients. The CSFs from three patients were tested for HBs-Ag and HBs-Ab. HBs-Ag was negative in all three patients, but HBs-Ab was positive in two patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

[A case of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) with bilateral recurrent nerve palsy and primary alveolar hypoventilation--comparative studies of the histological findings of the two sural nerve biopsies with 9 years interval].

A 27-year-old man noticed a tingling sensation in his fingers and toes in early 1982, at the age of 18 years, and his symptom gradually progressed in the following several months. In December 1982, based on neurological and laboratory examinations including the first sural nerve biopsy on the right side, a diagnosis of axonal sensory neuropathy of unknown etiology was made. During the following years, muscle weakness in the distal limbs and hoarseness developed and progressed, and the sensory impairments became gradually evident. On the second neurological examination in July 1991, he showed soft palate palsy and bilateral recurrent nerve palsy. The intrinsic muscles of hands and feet were atrophic, and pes cavus was noted bilaterally. There was mild to moderate weakness in the distal muscles of both limbs. Ankle jerk was absent and other tendon reflexes were decreased in both limbs. A mild to moderate decrease of both superficial and deep sensations with mild paresthesia was noted in both hands and feet. Routine laboratory findings were unremarkable. In blood gas analysis, hypercapnea and respiratory acidosis were found. Spirometry showed an increase of residual volume, and alveolar CO2-pulmonary ventilation response test suggested the presence of primary alveolar hypoventilation caused by hypofunction of the medullary respiratory center. In nerve conduction studies, motor nerve conduction velocities were moderately reduced in bilateral median and ulnar nerves. Distal latencies of M-waves were prolonged in bilateral median nerves. Temporal dispersion of M-wave was found in the left tibial nerve. The amplitudes of sensory action potentials were moderately reduced in bilateral median and sural nerves.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

[Atypical Guillain-Barré syndrome associated with ophthalmoplegia and visual impairment following herpes simplex virus type 1 infection].

Two weeks after a flu-like illness, a 59-year-old woman developed double vision, muscle weakness and sensory discomfort in the proximal portions of her limbs. On admission, there was complete external ophthalmoplegia with bilateral ptosis. The pupils were dilated and did not react to light. Swallowing and elevation of the soft palate were also limited. There was severe muscle weakness in all limbs. Deep tendon reflexes were absent. Superficial and deep sensations were impaired in the proximal portions of the extremities. Neuro-ophthalmological examinations revealed an acquired color disorder with no scotoma and normal discs. P100 latencies of flashed visual evoked potentials were prolonged on day 41, and returned to normal on day 87. Herpes simplex virus type 1 (HSV-1) infection was confirmed by isolation of the virus from her sputum and the detection of anti-HSV-1 antibody in the acute phase serum.

Female↗
PubMed1994

Contribution of neuromuscular impairment to physical functional status in patients with lumbar spinal stenosis.

OBJECTIVE: To evaluate the relationship between neuromuscular impairment and physical functional status in patients with lumbar spinal stenosis. METHODS: Cross sectional analysis of 217 consecutive patients with lumbar spinal stenosis referred to 3 teaching hospitals. Physical functional status was measured with the physical dimension of the Sickness Impact Profile (P-SIP). Physical and radiological findings were abstracted from clinical records. The neuromuscular findings included pin sensation, strength, deep tendon reflexes and vibration. They were aggregated in a neuromuscular impairment index (NMI). Univariate relationships of the P-SIP and the NMI were analyzed with nonparametric methods. The determinants of physical functional status were evaluated using multiple linear regression models. RESULTS: In 148 patients with complete clinical data, objective weakness of the lower extremity as measured at rest was not related to physical functional status in univariate analyses. Decreased vibration was common and was associated with balance disturbance and reduced physical functional status, reflecting the importance of proprioception loss. In the multivariate regression analysis, neuromuscular deficit explained only 2.5% of the variance in physical functional status. The primary determinants of physical functional status were pain, depression, comorbid conditions and work status. CONCLUSION: While neuromuscular impairment is an indispensable feature of the diagnostic evaluation, its value in assessing outcome is limited. The decision whether to intervene surgically in patients without cauda equina syndrome or rapidly progressive neurological deficits should therefore be driven by pain and physical disability rather than the degree of neuromuscular impairment.

Aged↗
PubMed1994

Acute and subacute organophosphate poisoning in the rat.

The intermediate syndrome in organophosphate poisoning is clinically characterized by weakness in the territory of cranial nerves, weakness of respiratory, neck and proximal limb muscles, and depressed deep tendon reflexes. It occurs between the acute cholinergic crisis and the usual onset of organophosphate-induced delayed neurotoxicity. The weakness has been ascribed to muscle fiber necrosis. Fenthion has been the most common cause. This study assesses the occurrence of the necrotizing myopathy in rats in relation to the clinical course and the acetylcholinesterase (AChE) inhibition after poisoning with organophosphates representative for each of the major types of organophosphate-related neurotoxicity. Marked differences are noted in the duration of cholinergic symptoms and of AChE inhibition after either paraoxon and mipafox, or fenthion poisoning. The necrotizing myopathy begins shortly after the initial decline in AChE activity with all organophosphates studied. Maximal muscle involvement occurs within the first 2 days of the poisoning with all organophosphates studied. The myopathy is not aggravated by a further decline in AChE activity in fenthion poisoning. Our data argues against the monophasic necrotizing myopathy being the cause of the intermediate syndrome, and is suggestive of persistent AChE inhibition being involved.

Animals↗
PubMed1994

[Crossed cerebello-cerebral diaschisis in olivopontocerebellar atrophy].

We reported a case of crossed cerebello-cerebral diaschisis (CCCD) in olivopontocerebellar atrophy (OPCA). A 49-year-old male was admitted with complaints of titubation, dysarthria and tremor. Examination on admission revealed exaggerated triceps, patella and achilles tendon reflexes on both sides and rigidity in left wrist. Ocular movements were slightly saccadic and speech was scanning or explosive. Finger-nose and heel-knee coordination was poor on both sides (left dominant). Cardiovascular reflex tests showed abnormal findings, suggesting insidious autonomic dysfunction. Brain CT and magnetic resonance imaging (MRI) revealed mild atrophy of the pons and cerebellum. Brain single photon emission computed tomography (SPECT) showed reduced cerebellar N-isopropyl-P-(123I) iodoamphetamine (IMP) uptake more prominent on the left than on the right side. A reduction of 123I-IMP uptake was more striking in the right thalamus, basal ganglia and frontal lobe than on the left side. The cerebellar sign which was left dominant and the left extrapyramidal sign were consistent with the side where reduction of 123I-IMP uptake was more prominent. We suggest that CCCD in our case resulted from transneuronal deactivation in the classic anatomical (cerebello-thalamo-cortical) pathway and dopaminergic (cerebello-basal ganglia-cortical) pathway. There is a possibility that CCCD reflects the development of pathological changes in OPCA.

Brain↗
PubMed1993

Clinical study of endemic cretinism in south Sikkim.

One hundred individuals suffering from Endemic Cretinism were studied. There were 55 males and 45 females. 62% of the cretins had visible goitre. Thirty nine (62.9%) goitrous cretins had grade II goitre. Neurological cretinism was the predominant type encountered (99%) and Myxoedematous cretinism was seen in only one patient. The most salient neurological feature was deaf-mutism seen in 74%. Findings in the motor system were, apart from deaf-mutism, the most characteristic feature of the condition on clinical examination. 58% had exaggerated deep tendon reflexes and 31% had extensor plantar response. Squint was noticed in 29%. Familial aggregation was noticed and was striking. Endemic cretinism is a distinctive and easily identifiable clinical entity and is an important indicator of the severity of iodine deficiency in a community.

Adolescent↗
PubMed1994

[Multiple sclerosis with syrinx formation in the spinal cord: a case report].

A 35-year-female developed tetraparesis following a period of back pain, urinary retension and paraparesis. She was admitted to our hospital on September 22, 1990. Neurological examination revealed tetraparesis with a sensory level at C3. Deep tendon reflexes were hyperactive in all four extremities with bilateral Hoffmann and Babinski reflexes. Spinal MR imaging demonstrated cavity formation within the cervical cord, extending from C2 to C6 without any anomalies at the craniocervical junction including Chiari malformation. The cavity was not enhanced with Gd-DTPA. Cerebrospinal fluid (CSF) examination revealed no abnormality. Although a syringo-subarachnoid shunt was performed on October 18, 1990, her symptoms did not improve. On December 17, 1990, she developed optic neuritis in the right eye and her paraparesis deteriorated. Delayed metrizamide CT scans showed another syrinx from Th3 to Th9. Repeated CSF contained 37 cells/mm3, protein 88 mg% and sugar 49 mg%. CSF oligoclonal bands were present and the CSF myelin basic protein was 6.6 ng/ml (normal < 4). A pulse therapy of steroid improved her vision and paraparesis. However, she developed paraparesis again on October 29, 1991. A brain T2-weighted MR image demonstrated multiple periventricular high signal intensity spots. Her paraparesis improved again with steroid. MR images in September, 1992 revealed a cord atrophy and disappearance of the cavity. Based on these clinical courses and radiological findings, a definite diagnosis of multiple sclerosis (MS) was made. We think MS may have caused the syringomyelia.

Adult↗
PubMed1994

Lambert-Eaton myasthenic syndrome in small cell lung cancer: nursing implications.

PURPOSE: To describe the pathophysiology and nursing care of patients with Lambert-Eaton myasthenic syndrome (LEMS), a little-known paraneoplastic syndrome. DATA SOURCES: Published articles, books and book chapters, and clinical trial experience. DATA SYNTHESIS: LEMS most commonly is associated with small cell lung cancer. Clinical presentation is characterized by weakness of the proximal muscles of the pelvis, thighs, shoulders, and arms and a weakening or absence of deep tendon reflexes. These symptoms are the manifestations of an abnormality at the neuromuscular junction and may precede the diagnosis of lung cancer. CONCLUSIONS: The oncology nurse knowledgeable about the pathophysiology, clinical features, diagnostic evidence, and treatment of LEMS is better able to care for and teach patients with this disorder. NURSING IMPLICATIONS: Nurses must assist patients in adjusting not only to a diagnosis of cancer and its treatment effects but also to the symptoms of LEMS, including impaired mobility, self-care deficits, and fatigue.

Adult↗
PubMed1994

[Hypothyroid myopathy. Communication of 4 cases].

We report four patients with primary hypothyroidism (3 female, aged 47, 46, 49 and 34 years old) whose principal manifestation was muscle involvement. The diagnosis was oriented by the finding of myoedema and a slow relaxation phase of tendon reflexes. In one patient, an electromyographic and histological study was performed. Thyroid substitution lead to an improvement in myopathy in all patients.

Adult↗
PubMed1993

Effects of human immunodeficiency virus and immune status on magnetic resonance imaging of the brain in hemophilic subjects: results from the hemophilia growth and development study.

To determine the effects of hemophilia and human immunodeficiency virus (HIV) infection on the nervous system, the authors examined the relationship of brain magnetic resonance imaging (MRI) findings to immunologic function and neurologic examination findings. Baseline examinations included physical and neurologic examination, immunologic and virologic testing, and MRI of the brain. On neurologic examination, muscle atrophy was considered to be related to hemophilia if adjacent joints had arthropathy due to bleeding. Muscle atrophy was considered non-hemophilia-related if unrelated to arthropathy or if muscle atrophy was diffuse. Subjects were boys aged 6 to 19 years, enrolled in a multicenter study of the effects of hemophilia and HIV infection on growth and development, all with congenital coagulopathies requiring factor infusions. Three hundred ten subjects had complete data including neurologic examination, T-cell subsets, HIV antibodies, and MRI. Subjects with HIV infection whose CD4+ counts were < 200/microL were compared with subjects with HIV infection and CD4+ counts > or = 200/microL and with HIV-negative subjects, all of whom had CD4+ counts > 200/microL. MRI studies were normal in 230. Abnormal MRI studies were more frequent in HIV-positive subjects with CD4+ counts < 200 (29.4% abnormal compared with 17% in HIV-positive subjects with CD4+ counts > or = 200 and 15.3% in HIV-negative subjects). Diffuse atrophy accounted for most of the excess abnormalities in HIV-positive subjects with CD4+ counts < 200 (77.3% of abnormal scans). Diffuse atrophy on MRI was associated with decreased muscle bulk on neurologic examination, but not with abnormal tendon reflexes.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1993

[Syringomyelic syndrome secondary to cervical canal stenosis and cervical spondylosis].

A 59-year-old man suffered from progressive muscular weakness and sensory loss of both upper limbs for seven years. Neurological examination revealed vest-form sensory loss of all modalities from the level of C3 to Th2 on both sides together with muscular weakness and atrophy of the upper limbs in predominantly proximal distribution. Deep tendon reflexes were generally hyperactive except for the left biceps brachii. Based on these neurological manifestations, a clinical diagnosis of syringomyelic syndrome was made. The plain X-ray showed anomalies of the craniovertebral junction; occipitalization of the atlas, separate odontoid and fusion of C2 and C3 vertebrae, as well as cervical canal stenosis with cervical spondylosis. On sagittal T2-weighted MRI, the spinal cord was compressed at multiple levels from C3/4 to C6/7, and an intramedullary high signal intensity area was demonstrated from the level of C1 to C3/4. T1-weighted axial image showed a cavity formation at the center of the cord from the level of C1 to C2. No chiari malformation was found. Normal pulsatile CSF movement was diminished below the level of compression on cine MRI. On delayed CT examination 6 hr after myelography, the contrast medium was collected inside the spinal cord and showed "snake-eyes" appearance at and near the level of spondylosis. Above this level extending to C1, there was a longitudinally oriented "pencil-shape" zone of intramedullary contrast collection. These neuroimaging findings well corresponded with the patient's neurological signs and symptoms. The muscular weakness of both upper limbs improved after conservative therapy including immobilization of the neck position.(ABSTRACT TRUNCATED AT 250 WORDS)

Cervical Vertebrae↗