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PubMed1999

[The clinical features of cervical spondylosis with boule musculaire].

To clarify the pathophysiology of boule musculaire associated with cervical spondylosis, we investigated the 13 patients (11 males and 2 females) with cervical radiculopathy caused by cervical spondylosis. None of the patients had any subjective symptoms such as sensory disturbance, weakness in the boule musculaire, and muscle atrophy of the insurround region near the boule musculaire. Among 21 tendon reflexes of the biceps muscle of the arm, 9 were normal, 8 were decreased and 4 were increased. Among the 13 patients there was only 2 clinical cases of cervical myelopathy. MRI obtained from 3 patients demonstrated a compressed cervical cord. Electromyography obtained from 7 patients demonstrated mild neurogenic changes such as polyphasic or prolonged motor unit potential (MUP) in the boule musculaire and in the atrophic regions. However, there was no giant MUP, fasciculation, fibrillation, nor positive sharp waves suggesting denervating lesions below the anterior horn in any patient. It was considered that the boule musculaire observed in cervical spondylosis gradually developed from a relatively mild disturbance of the ventral root. Moreover, the boule musculaire developed more often in the male patients, and predominantly on the right side. Cervical spondylosis accompanying boule musculaire may be a prodromal stage or a mild type of cervical spondylotic amyotrophy.

Aged↗
PubMedDate not supplied

Bilateral glaucomatocyclitic crisis in a patient with Holmes Adie syndrome.

A patient with pre-existing bilateral tonic pupils presented with simultaneous bilateral glaucomatocyclitic crisis. Deep tendon reflexes were absent although they were documented to be present 6 years ago. A possibility of a progressive autonomic dysfunction in both these conditions is discussed.

Adie Syndrome↗
PubMedDate not supplied

Clinical and neurophysiological correlations of spasticity.

The aim of this investigation was to explore the correlations between some neurophysiological methods and spasticity. An examination of 120 patients with spastic hemiparesis was performed. The muscle tone, force and tendon reflexes were assessed using well-known five-point scales. The F wave, T, H and flexor reflex parameters and the Hvibrated/Hmaximal ratio were obtained. Our results revealed moderate correlations (0.3 < r < 0.5) between the amplitudes of F wave, T and H reflexes and muscle tone. The correlations between the amplitude ratios (Fmaximal/M, Fmean/M, T/M, H/M) and muscle tone were poor, as were the correlations between H reflex thresholds and muscle tone. Moderate correlations existed between Hvibration/Hmaximal ratio and muscle tone. Only the second flexor reflex response showed moderate correlations with muscle tone. In conclusion correlations between the neurophysiological methods employed and muscle tone are moderate. Evaluation of all the F wave, T, H reflex and flexor reflex parameters is not necessary, as only some of these parameters show good correlations with spasticity.

Aged↗
PubMedDate not supplied

[Neurophysiological clinical study of 70 patients with type 2 spinocerebellar ataxia].

INTRODUCTION: The prevalence of hereditary ataxia in Holguín, Cuba, is 43 per 100,000 inhabitants, but in some regions reaches 503 per 100,000 inhabitants, a figure never previously recorded in the international literature. OBJECTIVES: To evaluate the part played by non-cerebellar structures and vias in causing some of the clinical signs of the disorder by means of clinico-electro physiological correlation. PATIENTS AND METHODS: A neurological examination, peripheral nerve conduction studies and somato-sensorial evoked potentials of the median and posterior tibial nerves were done in 70 patients with type 2 spinocerebellar ataxia. RESULTS: The commonest clinical signs were ataxia on walking, dysarthria, dysmetria and adiadochokinesia. Correlation analysis showed that the variable most significantly correlated with the degree of ataxia and Romberg's sign was latency of the P40 component, whilst tendon reflexes were best correlated with H reflex latency. However, the duration of the disease was not found to have statistical correlation. CONCLUSIONS: These results suggest that degeneration of long peripheral nerves and sensory paths contributes to the degree of ataxia and other clinical signs. At present no correlation has been found between the duration of the illness and increasing electrophysiological changes, and therefore seems not to have a major effect on neurodegenerative mechanisms.

Adolescent↗
PubMed1999

[Characteristics of computerized tomography of the brain in congenital hemiparesis].

Congenital hemiparesis is defined as an unilateral disorder of movement and posture, with clinical signs of spasticity with flexor hypertonicity, increased tendon reflexes and characteristic posturing. We have examined a group of 26 children with congenital hemiparesis (14 boys and 12 girls) with mean age of 3.5 years (range 6 months to 9 years). 24 had been born at term (% weeks gestation) and 2 were preterm (% completed weeks gestation). From the neuroimaging point of view, congenital hemiparesis form a rather heterogeneous group. CT scans revealed: porencephalic cyst (6), unilateral ventricular enlargement (2), cortical atrophy with unilateral ventricular enlargement (1), hypodense zones resulting from previous hemathermous (4), normal CT scans (6), and 7 cases have not had CT scans for technical reasons (war conditions). Congenital hemiparesis mainly affects term children with prenatal origin in majority of cases. Vascular occlusions (in utero stroke) originating from various pathophysiological factors, maternal or fetal, may result in congenital hemiparesis. Normal CT findings should be revised by using MRI, which provides direct evidence of white matter lesions.

Brain↗
PubMed2000

[A 77-year-old man with gait and gaze disturbance].

We report a 77-year-old Japanese man with progressive gait disturbance. He was well until his 71 years of the age (1992), when he noted an onset of disturbance in his speech, which was followed by difficulty in using his left hand. He did not attempt to use his left hand afterwards. He started to fall down in the spring of 1994. He was admitted to our service on October 6, 1994. Neurologic examination revealed an alert and oriented man. He showed limb-kinetic apraxia in his left hand with anosognosia for his apraxia. Vertical gaze was impaired. He walked in small steps. He had moderate axial and limb rigidity. He had no weakness, ataxia, or tremor. Deep tendon reflexes were normal. Plantar response was flexor. Sensation was intact. His gait had progressively become worse and he was admitted to another hospital in April of 1996. At that time he was disoriented to time. He was only able to walk a few steps with support. He continued to show limb-kinetic apraxia in his left hand. He developed dementia and dysphagia and he expired on October 27, 1998. He was discussed in a neurological CPC, and the chief discussant arrived at the conclusion that the patient had corticobasal degeneration. Most of the participants agreed with this diagnosis, but a few of them thought that progressive supranuclear palsy would be more likely. Post-mortem examination revealed no gross cortical atrophy. The right hemisphere was kept frozen for future biochemical analysis. The left precentral gyrus showed spongy changes, neuronal loss and gliosis. The pallidum, putamen, and the subthalamic nucleus were unremarkable, however, neurofibrillary tangles were seen in the subthalamic nucleus. The substantia nigra showed only slight neuronal loss; neuronal pigments were well retained. A few neurofibrillary tangles were seen in the remaining neurons. The cerebellar dentate nucleus showed grumose degeneration. Gallyas-Braak staining revealed many tuft-shaped astrocytes in the precentral gyrus. Pathologic diagnosis was progressive supranuclear palsy. Some participants thought that this diagnosis was unacceptable, because the pathologic changes in the substantia nigra, globus pallidus, and the subthalamic nucleus, which were usually severely involved in PSP, did not show typical changes of PSP. In addition, the predominant clinical feature was limb-kinetic apraxia, although he showed vertical gaze paresis and parkinsonian gait, which could also be seen in corticobasal degeneration. There was a big discussion among participants with regard to the diagnosis.

Aged↗
PubMedDate not supplied

Guanosine triphosphate cyclohydrolase I deficiency: a rare cause of hyperphenylalaninemia.

Tetrahydrobiopterin (BH4) deficiencies are a heterogeneous group of disorders caused by a defect in two of the three enzymes involved in its biosynthesis or in the two recycling enzymes. Except for the deficiency of dehydratase, an enzyme catalyzing a reaction in the recycling pathway, all other variants of BH4 deficiency are characterized by developmental delay, progressive neurological deterioration, hypokinesis, drooling, swallowing difficulty, truncal hypotonia, increased limb tone, myoclonus and brisk deep tendon reflexes. A deficiency of guanosine triphosphate cyclohydrolase I (GTPCH), the first enzyme in the biosynthetic pathway of BH4, is described in a 14-month-old male infant with hyperphenylalaninemia, developmental delay, hypertonia of the extremities, seizures, feeding difficulties, and vomiting. Urinary pteridine screening revealed very low levels of neopterin and biopterin which was highly suggestive of GTPCH deficiency. Low cerebrospinal fluid concentrations of 5-hydroxyindoleacetic acid (5HIAA) and homovanillic acid concentrations, together with no detectable neopterin and decreased concentrations of biopterin and folate, agreed with the diagnosis of GTPCH deficiency. Subsequently measured neopterin and biopterin synthesis in cytokine-stimulated skin fibroblasts confirmed GTPCH deficiency, albeit indirectly. The patient showed marked improvement on a low-protein low-phenylalanine diet with neurotransmitter precursor administration. The favorable outcome in this patient clearly shows that not only newborns with elevated phenylalanine levels but also older children with neurological signs and symptoms should be screened for a BH4 deficiency in order to have maximum benefit of the treatment.

Antioxidants↗
PubMed2000

Adult-onset nemaline myopathy and monoclonal gammopathy: a case report.

A 47-year-old female developed proximal limb weakness after hysterectomy for uterine fibromatosis. Muscle strength slowly improved, but relapse occurred at age 52. She presented with progressive gait difficulty, proximal limb weakness, and painful calves. Family history was not contributory. Cranial nerves, deep tendon reflexes, and sensation were normal. Serum creatine kinase was normal. An IgG kappa monoclonal protein was found. Nerve conduction studies were normal, but EMG showed brief small polyphasic motor unit action potentials with early recruitment in proximal muscles. Muscle biopsy showed abundant rods, atrophic muscle fibres, and type 1 fibre predominance. The sarcolemma was immunoreactive for IgG kappa. Plasmapheresis was unsuccessful, but methylprednisolone and azathioprine led to moderate improvement of muscle strength, associated with reduced monoclonal protein levels. This is the third case report, describing the association of monoclonal gammopathy and late-onset nemaline myopathy. Presence of a monoclonal protein at the sarcolemma and responsiveness to immunosuppressive treatment are suggestive of a dys-immune origin.

Age of Onset↗
PubMed2000

[A case of glioblastoma multiforme which indicated the early stage on brain MRI].

A 57-year-old male was urgently carried to our hospital because of sudden loss of consciousness, lasting about 10 minutes. He had resumed consciousness before he arrived at our hospital. Neurologically, he had mild muscle weakness of the right arm. Deep tendon reflexes in the right upper extremity were reduced. In high level functions, speech disturbance, dysgraphia (disturbed ability to write Hiragana), and constructive apraxia were noted. A brain MRI upon admission showed a poorly demarcated, high signal intensity area in the cortical and subcortical layers of the left temporal and parietal lobes. This was visible on T 2 weighted images(T 2 WI), although no abnormalities were visible on T 1 weighted images(T 1 WI). No contrast enhancement was effected by Gd-DTPA. The patient was therefore suspected of having a tumor or degenerative disease and was monitored closely. About 4 months later after onset, his symptoms became aggravated, and brain MRI disclosed a marked low signal intensity area on T 1 WI and a heterogeneous high signal intensity area on T 2 WI. The abnormal signal intensity area was surrounded by extensive edema and mass effect. Ring-shaped, irregular, contrast enhanced areas were also visible. Cerebral angiography revealed a poorly demarcated tumor stain in the area supplied by the middle cerebral artery. The tumor was removed surgically and was histopathologically rated as glioblastoma multiforme(GBM). Because this case represents a valuable example of early stage of GBM, it will be discussed in this paper, along with differential diagnoses.

Brain Neoplasms↗
PubMed2000

[An adult case of recurrent myelopathy presenting with monoplegia following asthmatic attacks].

A 22-year-old woman noticed an acute onset muscle weakness in her right leg after an asthmatic attack. A neurological examination showed moderate muscle weakness from the right iliopsoas muscle to the toe muscles, a decreased deep tendon reflex in her right lower limb and mild hypesthesia in her right L2-S1 segments. Needle EMG revealed fibrillation potentials in the right gastrocnemius muscle and a positive sharp wave in the right anterior tibialis muscle. The findings of motor nerve conduction studies and sensory nerve conduction studies were normal. The lesion was considered to be located at the posterior horns, as well as at the anterior horns at the L2-S1 levels and also at their roots on the right side. The anterior horn cells appeared to be the most severely affected. Polio-, echo-, entero- and coxsackie-virus antibody titers showed no significant changes on the 36th and 64th days of the disease. The serum IgE level was elevated and mite antigen-specific IgE was strongly positive. MRI revealed no abnormalities in either the thoracic or lumbar spinal cord. Although the sensory disturbance did rapidly improve after corticosteroid therapy, no improvement was seen in her muscle weakness which thus resulted in the atrophy of the affected muscle. While undergoing the corticosteroid therapy, she suffered another asthmatic attack. Nine days after the second attack, she further developed weakness in her right deltoid, biceps brachii, triceps brachii, wrist extensor, wrist flexor, digits extensor and digits flexor muscles with hyperreflexia in her left upper limb. Cervical MRI disclosed a high intensity area at the C3-6 level on the T2-weighted images and also a gadolinium enhancement of the lesion. Since monoplegia had appeared twice previously after bronchial asthma attacks in this case, Hopkins syndrome was suggested. Hopkins syndrome has so far been exclusively reported in children, and no recurrent cases have ever been reported with this condition. This is therefore considered to be the first case of Hopkins syndrome occurring in an adult and also demonstrating recurrence.

Adult↗
PubMed2000

[A patient with marked immunodeficiency in an HTLV-I carrier: a case report].

We report a 49-year-old man who was an HTLV-I carrier with an immunodeficiency state and intracranial pyramidal tract lesion revealed by MRI. He was born in Hokkaido and was admitted to our hospital because of fluminant hepatitis. On admission, neurologic examination revealed exaggerated deep tendon reflexes including the jaw jerk; the plantar response was flexor. Laboratory examination revealed decrease in the number of lymphocytes and CD4-positive lymphocytes in the peripheral blood and CD4/CD8 ratio was consistently low, indicating the presence of cellular immunodeficiency state. Serum anti-HTLV-I antibody was markedly increased but he did not have HTLV-I associated myelopathy (HAM). He had no underlying disease which would cause immunodeficiency state such as adult T-cell leukemia (ATL) or HIV infection. We concluded that the HTLV-I carrier state induced his immunodeficiency. During the course, he developed retrobulbar neuritis. T2 weighted cranial MRI revealed high signal lesions in the bilateral corona radiata, posterior limb of the internal capsule, and the pontine base, corresponding to the location of the pyramidal tracts. His hospital course was complicated by opportunistic infections such as Pneumocystis carinii pneumonia, cytomegalovirus infections, and meningitis, and died of multiple organ failure 7 months after the admission. Cellular immunodeficiencies in ATL patients are well known. Intracranial central nervous system (CNS) lesions in HAM patients are also mentioned. Recently coincidence of ATL and HAM in the same patients has also been reported. Asymptomatic HTLV-I carriers may have a latent immunodeficiency state and/or CNS lesions. We shall have to be alert about the presence of such carriers.

Carrier State↗
PubMed2000

[A case of motor neuron disease with dementia, presenting motor aphasia as an initial symptom].

We report a case of motor neuron disease (MND) with dementia, presenting motor aphasia as an initial symptom. A 67-year-old man was admitted to our hospital because of speech disturbance slowly progressing for 2 years. On physical examination, he showed no neurological abnormalities except for non-fluent aphasia and increased deep tendon reflexes without laterality. MRI demonstrated bilateral fronto-temporal atrophy, dominating the left hemisphere. This finding was confirmed by surface anatomy scanning (SAS), showing an obvious atrophy in the left inferior frontal gyrus, compared with the right one. SPECT with 123I-IMP revealed some irregular defects in the bilateral frontotemporal region. Because he showed dementia, bulbar palsy with tongue atrophy, weakness of upper extremities and facial muscles, snout reflex, and the atrophy and fasciculation in limbs in addition to motor aphasia soon after the discharge from our hospital, he was diagnosed as having MND with dementia. At age 68, he died of a respiratory failure 3 years after the onset of the disease. MND with dementia seldom shows motor aphasia as an initial symptom. We must include, however, the MND with dementia as an differential diagnosis when we see the patients with progressive aphasia.

Aged↗
PubMed2000

[A patient presented with atypical paroxysmal kinesigenic choreoathetosis and Becker muscular dystrophy].

A 22-year-old man had choreatic movements in upper limbs, neck and trunk for over twelve years which were associated with dystonia in lower limbs upon initiating voluntary movements. The choreatic movement lasted for a few seconds and the dystonia lasted for a few minutes. He also had high serum CK levels and hypertrophic calf muscles. His muscle strength and deep tendon reflexes were normal. His choreatic movements fulfill the criteria for paroxysmal kinesigenic choreoathetosis (PKC). However, it was unclear what the symptom of dystonia was due to. From a muscle biopsy and DNA analysis, he was diagnosed as having Becker muscular dystrophy. Administration of anticonvulsant improved the dystonia as well as the choreatic movement, which showed that the dystonia was a symptom of PKC. Coincidence of choreatic movements and dystonias which had different lasting time in a patient of PKC was atypical and had not previously reported.

Adult↗
PubMed2000

[A case of atopic myelitis].

A 35-year old woman was admitted to our hospital because of slowly increased numbness of lower truncus and the legs for 10 months. She showed atopic dermatitis on her nape and bilateral popliteal fossa, and signs and symptoms of anorexia nervosa, such as asitia, emaciation, and menopause. Neurologic examination revealed Lhermitte's sign, muscle weakness of bilateral hands, deep and superficial sensory disturbance below the Th 4 level of thoracic spinal cord, and increased tendon reflexes of four limbs. Laboratory data showed hyperIgEemia and high titer of mite antigen specific IgE in sera. Cervical MRI demonstrated abnormal intensity area located at the C6 to C7 segments (i.e. low intensity in T1 weighted images and high in T2). She also showed hypercalcemia and swelling of the parathyroid gland, and had been diagnosed primary hyperparathyroidism by scintigram of the parathyroid gland. We concluded that this case is thought to be atopic myelitis, which has been recently reported as acute myelitis associated with hyperIgEemia and atopic dermatitis proposed by Kira et al. (1997). The patient also had anorexia nervosa and primary hyperparathyroidism.

Adult↗
PubMed2000

[A case of Guillain-Barré syndrome (GBS) following human parvovirus B19 infection].

Human parvovirus B19 (HPV-B19) infection is recently known to produce variable clinical manifestations, but neurological disorder associated with this infection is uncommon. We reported a case of GBS associated with transient lupus-like status following HPV-B19 infection. This is the first report describing an adult case of GBS following HPV-B19 infection. A healthy female, aged 33, developed erythema infectiosum simultaneously with her 5-year-old daughter. On the same day, she noticed leg fatigue, which worsened in the following days. On the day 11th, she became unable to walk. Mild pancytopenia, liver injury, proteinuria, hypocomplementemia, and increased anti-nuclear antibody (ANA) were revealed at a hospital. Polymerase chain reaction detected HPV-B19 DNA in the serum. On the day 17th, she was admitted to our hospital because of moderate generalized weakness and mild sensory disturbance, which were symmetrical and distal-dominant. The deep tendon reflexes were absent. Analysis of cerebrospinal fluid showed albuminocytologic dissociation. Other laboratory data were normal except positive ANA. Enzyme-linked immunosorbent assay (ELISA) showed high titer of the serum IgM antibody to GM1 and GD1b. Serum anti HPV-B19 IgM and IgG tested by ELISA were also positive. She improved gradually after 2 courses of double filtrated plasma pheresis.

Adult↗
PubMed2000

[Neurosarcoidosis with girdle sensation and polyradiculoneuropathy masquerading as Guillain-Barré syndrome].

We herein report two patients with neurosarcoidosis presenting girdle sensation in the trunk and polyradiculoneuritis. The first patient, a 53-year-old woman, manifested subacute progressive paresthesia in all four limbs and below the Th 3 level with girdle sensation from the thorax to lower abdomen and mild weakness in the left upper limb and the bilateral lower limbs. The patient was diagnosed to have sarcoidosis based on a biopsy of the scalenus anticus lymph nodes. The second patient, a 63-year-old woman, showed an acute onset of weakness and paresthesia in all four limbs and girdle sensation from the Th 5 to Th 8 level. On examination, she demonstrated diminished tendon reflexes in all four limbs, mild to severe weakness in all four limbs, paresthesia in all four limbs and below the Th 5 level. Although Guillain-Barré syndrome was initially suspected in this patient, the presence of girdle sensation led us to examine the possibility of neurosarcoidosis. Her examination demonstrated an abnormal accumulation of gallium in the bilateral hilar lymph nodes and mediastinum on scintigraphy, an elevated CD 4/CD 8 ratio in the bronchoalveolar lavage fluid, a negative tuberculin reaction, and elevated serum lysozyme level. These findings thus fulfilled the clinical criteria for sarcoidosis. None of the two patients showed any abnormalities in the thoracic cord MRI. In the first patient F wave was not evoked in either upper or lower limbs, while in the second patient temporal dispersion on M wave was observed in the right median and both ulnar nerves. We therefore consider the girdle sensation to have not been caused by myelopathy but instead by polyradiculopathy. When sarcoid peripheral neuropathy masquerades as Guillain-Barré syndrome, then the presence of girdle sensation may help diagnosis of neurosarcoidosis.

Diagnosis, Differential↗
PubMed2000

[A young adult female case of Wilson's disease presenting with mental disorder and frontal lobe signs].

We report a young adult female case of Wilson's disease presenting with mental disorder and frontal lobe signs. The patient was admitted to our neurological unit on October 4, 1999 because of schizophrenia-like symptom, dysphagia, dysarthria and gait disturbance. She showed slowly progressive rigidity and dystonia. Her parents were the second cousins. Neurological examination revealed bilateral pyramidal and extrapyramidal signs, frontal lobe signs (include the imitation behavior). Tendon reflexes were slightly exaggerated in all extremities. Bilateral Babinski, Chaddock and Hoffmann signs were positive. Her verbal IQ on the Wechsler Adult Intelligence Scale-revised was 49. Biochemical examination revealed low plasma copper and ceruloplasmin concentration. Cerebrospinal fluid was normal. Cranial MRI demonstrated diffuse brain atrophy and enlargement of the lateral ventricles. T2-weighted images of the MRI demonstrated hyperintense signal in both thalamus and basal ganglia. SPECT showed hypoperfusion in the left frontal lobe, both thalamus and basal ganglia. EEG revealed diffuse theta wave. The diagnosis of Wilson's disease was made and the treatment of D-penicillamine 900 mg per day was started. This hypoperfusion of SPECT and EEG findings improved after 2 months under D-penicillamine therapy. Neurological findings showed slight improvement. A few Wilson's disease patients presenting with mental disorder have been reported. Wilson's disease should always be considered in differential diagnosis of mental disorders. We emphasize the importance of early diagnosis and treatment of Wilson's disease.

Adolescent↗
PubMed2000

[A case of acute quadriplegic myopathy].

A 22-year-old man developed unconsciousness, severe quadriplegia and muscle atrophy, and had markedly elevated serum creatine kinase levels after using the high-dose steroid and nondepolarizing neuromuscular blocking agents during the course of sepsis and DIC. On neurological examination, he was lethargic. The patient had generalized muscle weakness and wasting, and diminished deep tendon reflexes. He weakly responsed to painful stimuli on the legs. The motor nerve conduction study demonstrated decreased CMAP (compound muscle action potential) amplitudes. Motor and sensory nerve conduction velocities and their distal latencies were normal. Muscle biopsy revealed marked muscle fiber atrophy predominantly in type 2 fibers and numerous basophilic and a few necrotic fibers. Some atrophic fibers had decreased to absent myosin adenosine triphosphatase activity in their center. Accordingly, he was diagnosed as having acute quadriplegic myopathy (AQM), which has been reported mainly in Western countries. The mechanism of muscle fiber degradation in this myopathy is still unknown. On immunohistochemical analysis to our patient, enzyme activities of various proteases such as calpain, cathepsin B, and proteasomes were increased in the sarcoplasm, especially in the atrophic fibers. We suggest that lysosomal cathepsin, nonlysosomal calpain, and ATP-ubiquitin-proteasome proteolytic pathways participate in muscle fiber degradation in AQM.

Acute Disease↗