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PubMedDate not supplied

Dissection of aorta: a pediatric case report.

We present a 15-year-old boy who developed sudden walking disability and sensory loss. He could not stand up on his feet and had no feeling following a sudden fall while playing basketball. He had been referred to a local hospital with these symptoms. In his physical examination absence of deep tendon reflexes and sensory loss were noted. His arterial blood pressure was 210/160 mmHg. He was transferred to our hospital with these findings and diagnosis of Guillain-Barré syndrome and hypertensive encephalopathy. There was sudden onset of sensory loss, walking disability and history of trauma. In the following hours hematuria, back pain and lower extremity ischemia developed. We suspected spinal artery injury based on the findings. Dissection of descending aorta was established with the help of magnetic resonance imaging of spinal region and contrasted aortography. The patient went to surgery immediately. He was lost on the second day after operation because of malperfusion. We report this case because dissecting aorta is very rare in the pediatric age group. High index of suspicion and early aortography are needed to diagnose aorta dissection.

Adolescent↗
PubMed2002

[A case of brachial plexus neuropathy who presented with acute paralysis of the hand after sleep].

We report a 46-year-old woman who presented with acute paresis of the right hand and arm. She was well until when she noted a paresis and dysesthesia in her right hand in the morning. Neurological examination revealed weakness in the muscles which were supplied by lower cervical segments, with increased deep tendon reflexes in the right arm. Allen's test and Wright's test were positive. The nerve conduction studies disclosed a reduced CMAPs more severely by right median than ulnar nerve stimulation. The frequency and amplitude of the F waves was also reduced. Needle electromyogram showed a mild neurogenic pattern in the right hand muscles. Digital subtraction angiography revealed a tapering of the subclavian artery when the right arm was abducted. She underwent decompression surgery. A remarkable improvement of the symptoms was observed after surgery. Our patient suggests that brachial plexus neuropathy should be considered in the acute paresis of the hand after sleep, and that surgical procedure would lead to a successful outcome.

Acute Disease↗
PubMed1976

Biofeedback treatment of foot drop after stroke compared with standard rehabilitation technique (part 2): effects on nerve conduction velocity and spasticity.

Peroneal nerve conduction velocity (NCV) was determined in 20 hemiplegic patients with chronic foot drop. At the initial visit, relative slowing of NCV of the affected leg was observed. The patients were randomly separated into two groups, and treated for five weeks by different therapies--group 1 by conventional physical exercise and group 2 by physical exercise plus biofeedback training. Of these patients, six with severe spasticity were selected from each group to investigate the change of spasticity by patellar tendon reflex. Although with biofeedback remarkable improvement of function was observed (and reported in an earlier paper), there was no significant change of NCV and spasticity.

Autonomic Nervous System↗
PubMed2002

[A case of CIDP with horizontal gaze-evoked nystagmus and ataxia].

A 46-year-old man developed mild to moderate weakness in the distal muscles of lower limbs and then had gradually progressive weakness and sensory loss in four limbs. He subsequently developed difficulty in walking over a few months. Examination showed severe distal muscle weakness and atrophy, but mild proximal weakness in four limbs. Superficial sensation was decreased in both distal limbs and his vibratory sense was mildly decreased in bilateral feet. All tendon reflexes were absent. Furthermore, he showed four-limb and truncal ataxia with bilateral horizontal gaze-evoked nystagmus in both directions. Nerve conduction study revealed sensorimotor neuropathy, and sural nerve biopsy showed mixed axonal damage and demyelination. Cerebrospinal fluid protein levels were raised 212 mg/dl. Lumbar spine MRI showed marked cauda equina enhancement with gadolinium. Anti-ganglioside antibodies were negative but serum antineuronal antibodies without known antigen specificity were found. Neurootological findings indicated bilateral horizontal gaze-evoked nystagmus was caused by spinocerebellar damage. We diagnosed this case was CIDP with cerebellar ataxia. After administration of high dose steroid therapy, intravenous methylprednisolone 1000 mg/day, his symptoms including ataxia and polyneuropathy were apparently improved.

Gait Ataxia↗
PubMed2002

[Ptosis and mastication disorders revealing concurrent myasthenia gravis and chronic polyradiculoneuritis].

Although myasthenia gravis (MG) has frequently been associated with other autoimmune disorders, it has only rarely been reported in conjunction with diseases of the nervous system. A 74-year-old patient with hypertension suddenly presented left unilateral ptosis and mastication disorders. Clinical examination showed a concomitant loss of strength distally and reduced deep tendon reflex. Electrophysiologic data indicated a diagnosis of MG and chronic inflammatory demyelinating polyneuropathy; acetylcholine receptor antibody was elevated at 4.1 nmol/L (normal < 2 nmol/L). Improvement was rapid after initiation of pyridostigmine in association with corticosteroid (1 mg/kg/day). One month later, the cranial nerve deficit disappeared and strength was normal. It is likely that a basic abnormality of immune regulation was responsible for the emergence of diseases with different clinical presentations, but similar immunopathogenesis. Corticosteroid seemed to be the most effective treatment.

Adrenal Cortex Hormones↗
PubMed2002

[A case of Gitelman's syndrome presenting with the hypokalemic periodic paralysis].

We report a rare case of Gitelman's syndrome (GS) presenting with the hypokalemic periodic paralysis. A 27-year-old man was admitted to our hospital because of transient weakness of the limbs. Past history was unremarkable, including the delivery and early developmental milestones, except for a transient limb weakness 7 times since the age of 15 years. The blood pressure was 140/90 mmHg. The physical examinations were unremarkable. Neurologically, the patient was fully oriented. The cranial-nerve functions were intact. Manual muscle tests revealed 1/5 weakness in his neck and extremities. Sensation was normal in all modalities. The deep tendon reflexes were present but decreased mildly. Laboratory tests showed hypokalemia (1.9 mEq/l), hypomagnesemia (1.8 mEq/l), and hypocalciuria (40.0 mg/dl). Plasma rennin activity and aldosterone concentration were elevated. The molar ratio of urinary calcium/creatinine was 0.11 (< 0.2). Arterial blood gas showed mild metabolic alkalosis with respiratory compensation. Because of these data, the diagnosis of GS was made. Gene mutations in the renal thiazide sensitive Na-Cl cotransporter (TSC) have already been shown to cause GS. Although we searched for gene mutation of TSC, none of 25 mutations in 18 out of 26 exons which had been previously reported were found. This is the first report of Gitelman's syndrome presenting with the hypokalemic periodic paralysis in Japan.

Adult↗
PubMed2002

Neurologic and cardiac progression of glycogenosis type VII over an eight-year period.

Little is known about the progression of phosphofructokinase deficiency (glycogenosis type VII, Tarui's disease). We describe a 66-year-old woman who had this disease diagnosed in 1997. Initial manifestations had included simple partial seizures since 1977, anginal chest pain since 1982, and muscle cramps since 1983. To prevent recurrent myocardial infarction, anticoagulation therapy with phenprocumon was initiated. Cardiac involvement progressed over an 8-year period, manifesting as low-voltage electrocardiogram (ECG), ectopic supraventricular tachycardia, thickened mitral valve, mitral valve insufficiency, enlarged left atrium, left ventricular hypertrophy, and diastolic dysfunction. Progression of neurologic involvement manifested as complex partial seizures, double vision, reduced tendon reflexes, central facial palsy, bradydiadochokinesia, and distal weakness of the upper extremities. Discontinuance of oral anticoagulation after 19 years, initiation of enalapril therapy, and administration of carbamazepine markedly improved the patient's condition.

Aged↗
PubMed2002

[A case of thoracic spondylosis presented with an attack of abnormal sensation and hyperhydrosis on the upper back].

A 23-year-old man presented an attack of abnormal sensation and hyperhydrosis on his upper back when he was tense or took a bath. This presentation continued for a month after commencement of Judo practise. Neurological examination found hyperactivity of bilateral deep tendon reflex alone. Magnetic resonance image demonstrated that the anterior thoracic spinal cord at the Th 4/5, 5/6 and 7/8 level were compressed by a bony spur. In our case, limitation of exercise, and prescription of adenosine triphosphate disodium and vitamin B led to a favourable outcome. Thoracic spondylosis in a young person is rare and there have been no standard protocols for the treatment. Thus, further clinical investigations are warranted.

Adult↗
PubMed2003

Neurological manifestations of HIV infection.

Case records of HIV infected patients were analyzed for identifying neurological manifestations. Eight patients (7 males) were identified to have probable HIV encephalopathy (in a period of 24 months) as per the CDC revised classification system. Their ages ranged from one year to ten years. The neurological manifestations noted included-developmental delay (2 cases), seizures (6 cases), acute onset alteration of sensorium (4 cases), aphasia (2 cases), loss of vision (2 cases), focal neurological deficits (6 cases), brisk deep tendon reflexes (7 cases), extensor plantar responses (5 cases) and signs of cerebellar dysfunction (2 cases). Other clinical features included growth failure, microcephaly, fever, lymphadenopathy, hepatomegaly, splenomegaly, pneumonia, otorrhea and oral candidiasis. Cerebrospinal fluid studies were normal. The neuroimaging features included cerebral atrophy and ventricular dilatation, cerebral infarction, basal ganglia calcification and cerebellar atrophy. Childhood HIV infection may have a variety of neurological abnormalities. HIV infection should be suspected in children presenting with unexplained neurological manifestations and growth failure.

Child↗
PubMedDate not supplied

[Guillain-Barre's syndrome in childhood (author's transl)].

Seventeen cases of Guillain-Barré's syndrome aged between 14 month ans 7 years are studied from clinical, analytical and evolutives aspects. Neither sex nor season predominance occurs. Sixteen of the patients had a previous viral or bacterial infection. Difficulty in walking was the main symptom at the onset of illness. Arreflexia and motot paralysis were always symmetrical and ascending. Albumino-cytological dissociation in the C.S.F. was found in the whole group. An evolutive study was made of the recovery of movement, C.S.F. and tendon reflexes which occurred in this order except in two cases which showed abnormal evolution. We emphasize the extent and frequency of respiratory difficulties at the onset of illness. Some etiopathogenic aspects, the lack of specifity of the syndrome and the differences of the diagnosis with that of poliomyelitis are commented. We point out the lack of effect of the corticosteroids treatment and the positive effects of phisiotherapy after the acute stage.

Cerebrospinal Fluid Proteins↗
PubMed2002

[A patient of sensorimotor neuropathy with small cell lung carcinoma and anti-GM1 antibody].

We reported a 62-year-old woman had sensorimotor neuropathy with small cell lung carcinoma (SCLC) and anti-GM1 antibody. She was admitted with several months history of progressive numbness, walking disturbance and anorexia. Neurologic examination revealed severe numbness and deep sensory disturbance of extremities and body, and mild weakness of distal extremities. Deep tendon reflexes were absent. Her limbs were ataxic. Nerve conduction studies showed no sensory evoked responses. CSF protein was elevated. Sural nerve biopsy revealed severe loss of myelinated fibers and perivascular mononuclear cells surrounding the perineurial vessel. Vasculitic neuropathy was diagnosed, and prednisolone was started, with no benefit. In the clinical course, she developed cough attacks and was found the lymphnode swelling in the mediastinum and supraclavicular fossa, which was diagnosed SCLC. Although anti-Hu antibody were not detected, anti-GM1 antibody was positive. She was treated with intravenous immunoglobulin, with transient improvement. The rare case of the paraneoplastic peripheral neuropathy with SCLC and anti-GM1 antibody was reported.

Autoantibodies↗
PubMedDate not supplied

Late-onset distal polyneuropathy due to acute organophosphate intoxication case report.

Intoxications due to organophosphate insecticides are common in our country, since agriculture has an important place. Besides the well known acute cholinergic toxicity, these compounds may cause late-onset distal polyneuropathy occurring two to three weeks after the acute exposure. An eight-year-old boy and a 13-year-old girl admitted to the hospital with gait disturbances. Beginning 15 and 20 days, respectively, after organophosphate ingestion. Neurologic examination revealed bilateral dropped foot, absent Achilles tendon reflexes and peripheral sensory loss. Electromyography demonstrated motor weighed sensory-motor polyneuropathy with axonal degeneration significant in the distal parts of bilateral lower extremities. Biochemical, radiological findings and magnetic resonance imagings were normal. The two cases were taken under a physiotherapy program. The two cases are presented here since organophosphate poisonings are common in our country, and since late-onset polyneuropathy is not a well known clinical presentation as acute toxicity.

Adolescent↗
PubMed2002

[A case of pseudomigraine with pleocytosis].

We report a case of pseudomigraine with pleocytosis (PMP) characterized by temporary neurological deficits and elevated cell counts in cerebrospinal fluid (CSF). A 28-year-old woman was admitted to our hospital with a second episode of right side throbbing headache accompanied by hemianopsia without scintillating scotoma of left side, hand numbness and weakness of left hand. Two months before the admission, she experienced a first identical episode, which lasted several hours. On admission to our hospital, neurological examination showed left hemianopsia, mild left hemiparesis, dysesthesia of left hand, exceeded tendon reflex of left upper limb, stiff-neck and positive Kerning's sign. CSF examination showed mild elevation of mononuclear cell counts. No abnormal findings on brain CT and MRI (including diffusion weighted image) were observed. 99mTc-HMPAO single photon emission computed tomography (SPECT) demonstrated extensive hypoperfusion at right cerebral hemisphere, corresponding to her neurological deficits. Her electroencephalography (EEG) showed reduced amplitude on the right occipital area. The reduced amplitude of cortical component of somatosensory evoked potential (SEP) by left median nerve stimulation were observed. On the third day after the admission, her symptoms improved and cell count of CSF was normalized. One week after the onset her SEP, EEG and SPECT were normalized on their retrials. She has never recurred these symptoms. We established a diagnosed of psedomigraine with pleocytosis as the first Japanese case.

Adult↗
PubMedDate not supplied

Atypical paraneoplastic syndrome associated with anti-Yo antibodies.

OBJECTIVE: Polyneuropathy, myopathy and spasticity have not been described as a manifestation of a neurologic paraneoplastic syndrome (NPS) associated with anti-Yo antibodies (anti-Yo). CASE HISTORY: The patient is a 60-year-old woman with a history of ovarectomy, salpingectomy, hysterectomy and omentectomy because of ovarian cancer with peritoneal carcinosis. From May to September 1999, she received chemotherapy with carboplatin and docetaxel. In June 1999, weaknesses of the lower limbs began to appear. Neurologic investigation revealed bilateral ptosis with right-sided predominance, exaggerated deep tendon reflexes, discrete distal weakness, wasting of the upper limbs and diffuse weakness of the lower limbs. She had slight CK elevation, elevated lactate dehydrogenase and aldolase levels. Testing for anti-neuronal antibodies revealed high serum titers of antibodies against the cytoplasm of Purkinje cells, confirmed as anti-Yo by immunoblot with recombinant proteins. CSF investigations showed 12/3 cells and positive oligoclonal bands. MRI of the brain showed bilateral, old ischemic basal ganglia lesions exclusively. Visually evoked potentials gave prolonged P100 latencies bilaterally. Nerve conduction studies and electromyography revealed motor polyneuropathy of the lower limbs. Muscle biopsy from the right anterior tibial muscle showed non-specific myopathic features. CONCLUSION: Polyneuropathy, myopathy and tetraspasticity may be the exclusive manifestations of an atypical NPS associated with anti-Yo. Anti-Yo may persist for years without relapse of the primary tumor.

Antibodies↗
PubMed2003

[Guillain-Barré syndrome in patients treated for Hodgkin disease].

INTRODUCTION: A 14-year-old boy treated with Hodgkin's disease developed muscular weakness and pain, hypotonia, abolished deep tendon reflexes. Examination of the cerebrospinal fluid showed albuminocytologic dissociation, the characteristic finding of Guillain-Barré syndrome. After high dose steroid treatment complete recovery occurred. DISCUSSION: Paraneoplastic neuropathies may develop in patients with cancer, Guillain-Barré syndrome occurs in patients with active Hodgkin's disease. CONCLUSIONS: Progressive neurological signs may indicate the presence of a malignancy, or in case of chemotherapy shows the activity of the tumour.

Adolescent↗
PubMed2003

Do we consider Andermann syndrome in infants with agenesis of corpus callosum.

Andermann syndrome is characterized by agenesis of corpus callosum, anterior horn cell disease, a mixed sensory and motor neuropathy, and facial dysmorphism, and is inherited as an autosomal recessive trait. A 7-month-old boy was admitted with developmental retardation. Head control was not gained and he could not sit. He had high arched palate, elongated facies and large angle of the mandible, which were compatible with the Andermann syndrome. Moderate hypotonicity and absent tendon reflexes were also noted. Serum creatine kinase level was normal. Magnetic resonance imaging of the brain showed agenesis of the corpus callosum. Electromyographic examination revealed the presence of both sensory and motor neuropathy. The patient was diagnosed as having the Andermann syndrome according to the clinical and laboratory findings and he is reported due to rare presentation.

Agenesis of Corpus Callosum↗
PubMed2003

A fatal case of cerebellar hypoplasia associated with anterior horn cell disease.

A 27-month-old girl was admitted with inability to walk and speak. The pregnancy, labor and delivery were unremarkable. She was the second child of first degree consanguineous parents and the other 5-year-old child was healthy. On physical examination, she could sit without aid. Horizontal nystagmus and bilateral optic atrophy were diagnosed. Moderate hypotonicity and muscle atrophy were noted in the lower extremities, and deep tendon reflexes were found to be brisk. Serum creatine kinase level was normal. Brainstem auditory evoked potential was also bilateral normal. Flash visual evoked potential was found to be prolonged bilaterally. Magnetic resonance imaging of the brain showed severe cerebellar hypoplasia and mild cerebral atrophy. Electromyographic examination was consistent with anterior horn cell disease. Muscle biopsy specimen was unremarkable. Genetic analysis was unremarkable. The patient was diagnosed with cerebellar hypoplasia associated with anterior horn cell disease, which was named as amyotrophic cerebellar hypoplasia, Norman's disease or infantile neuronal degeneration in the literature. During the follow-up, the parents said that she died at the age of 34 months, because of probable infection.

Cerebellum↗
PubMed2003

[High-dose intravenous immunoglobulin therapy in a child case of Bickerstaff's brainstem encephalitis].

We report an 11-year-old boy with Bickerstaff's brainstem encephalitis (BBE). He had gait disturbance, disturbed consciousness, and diplopia after upper respiratory tract infection. On admission, he showed multiple cranial nerve palsy, muscle weakness of arms, cerebeller ataxia and generalized areflexia. The cerebrospinal fluid on day 7 revealed albuminocytologic dissociation. IgG antibodies against GQ1b and GT1a were detected in the serum. Immunoglobulin was administered intravenously from day 11, and then his symptoms gradually diminished. When he was discharged on day 27, he had neither conscious disturbance nor limb weakness. There still were mild ophthalmoparesis and diminished deep tendon reflexes, but they disappeared by 10 months after the onset. Effective therapy for BBE has yet to be established. Our case had features of Guillain-Barré syndrome (GBS) and Miller Fisher syndrome, such as an acute monophasic course, limb weakness with areflexia, albuminocytologic dissociation in the cerebrospinal fluid, detection of serum anti-ganglioside antibodies and efficacy of intravenous immunoglobulin, indicating that BBE and GBS are closely related. Our case suggested that intravenous immunoglobulin therapy, an established treatment for GBS, should be considered in some patients with BBE.

Autoantibodies↗