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PubMed1997

[A case of spastic tetraplegia with medullo-cervical atrophy].

A 48-year-old man, who had spastic tetraplegia and a marked atrophy of the medulla oblongata and upper cervical cord, was reported. He began to walk in spastic fashion at the age of 12 years, and was diagnosed as spastic paraplegia. His father, whose onset of the disorder was 35 years old and died of pneumonia at the age of 69 years, manifested symptoms and a course, both resembling those of the present patient. Generalized weakness progressed gradually, and the patient was confined to bed in his forties. On admission, he showed markedly increased tendon reflexes and pathological reflexes in all the extremities. Muscular weakness was severe in the neck, trunk and extremities, and mild in the facial muscles. There were neither bulbar sign, significant respiratory failure nor fasciculation of muscles. A needle EMG examination revealed no apparent neuropathic findings. MR imaging showed a marked atrophy of the medulla oblongata and upper cervical cord, which was not considered to be secondary to vascular or infectious diseases. Though sensory evoked potentials showed no response at the latencies of central nervous components, visual evoked potentials, brainstem auditory evoked response and blink reflex were normal. This case might represent an unknown hereditary degenerative disease with autosomal dominant inheritance.

Humans↗
PubMed1997

[Angiostrongylus in the infant at Reunion and Mayotte. Apropos of 3 cases of eosinophilic meningitis including 1 fatal radiculomyeloencephalitis with hydrocephalus].

BACKGROUND: Eosinophilic meningitis caused by Angiostrongylus cantonensis is widespread in Southeast Asia and Pacific islands. Adults develop a transient meningitis with a benign course but severe or fatal disease may occur in pediatric patients. CASE REPORT 1: A 11 months old boy living in Mayotte island was hospitalized some days after fever and skin rash with seizure status, coma, flaccid quadriplegia, absence of deep tendon reflexes, urinary retention and anal incontinence. Eosinophilia was observed in peripheral blood and in the cerebrospinal fluid. Secondary, he developed a triventricular hydrocephalus treated by a ventriculoperitoneal shunt. After 3 weeks, the child died. Retrospectively, the diagnosis of angiostrongylus infection was established with the help of serology. CASE REPORTS 2 AND 3: Two infants, 10 and 11 months old boys, living in Reunion island, developed fever and vomitings, irritability and, for one of them, a unilateral sixth cranial nerve palsy. There was eosinophilia in the peripheral blood and in the cerebrospinal fluid. All symptoms progressively disappeared with complete recovery. The suspected diagnosis of angiostrongylus infection was confirmed by the serology. CONCLUSION: We report the first case of Angiostrongylus cantonensis infection in the French island of Mayotte (Comoro Islands) and we confirm the presence of this disease in Reunion island. In this Indian Ocean area, eosinophilic meningitis occurs most of the time in infants with sometimes severe radiculomyeloencephalitic forms. The origin of these occasionally massive infections is the giant African snail Achatina fulica. For a child with meningitis living in Reunion or Mayotte, or coming back from these 2 islands, Angiostrongylus cantonensis infection must be evoked, especially if there is a blood eosinophilia. Since efficiency of antiparasitic treatment is nowadays not proved, information must be given to people living in exposed areas in view to limit incidence of this disease.

Angiostrongylus cantonensis↗
PubMed1998

[Acute transverse myelitis presenting with syrinx formation associated with anti-sulfated glucuronyl lactosaminyl paragloboside antibody and anticardiolipin antibody].

A 37-year-old woman was admitted because of rapidly progressive unsteady gait, back pain and ascending dysesthesia below the lower chest level. On admission, she showed ataxic gait, positive Romberg's sign, severely impaired deep sensation of lower extremities, and vesico-rectal disturbance. Deep tendon reflexes in both lower extremities were brisk, while normal in the upper extremities. Babinski's sign was positive on both sides. On laboratory data, antinuclear antibody, immune complex and the low titer of IgG anticardiolipin antibody as well as IgM anti-sulfated glucuronyl lactosaminyl paragloboside (SGLPG) antibody were positive in her serum. Cerebrospinal fluid showed pleocytosis and increased protein level, but no oligoclonal IgG bands. The posterior tibial nerve SEP showed no P39 peak with normal latency of N20. Spinal MRI revealed mild cord swelling and syrinx formation at T7 to T9 level. Steroid therapy including pulse therapy with methylprednisolone was effective. The present case was diagnosed as acute transverse myelitis (ATM) similar to lupoid sclerosis, and to the best of knowledge, the first case of ATM with anti-SGLPG antibody. It is speculated that the autoimmune mechanism with anti-SGLPG antibody and anticardiolipin antibody by reacting with the endothelial cells in the central nervous system might contribute to causing ATM in our case.

Acute Disease↗
PubMed1997

Propofol anesthesia in a patient with Isaacs syndrome--report of a case and literature review.

Isaacs syndrome is an unusual lower motor neuron disease characterized by myokymia (muscle twitching), muscular stiffness, and decreased tendon reflexes. We reported a patient who was affected with this rare disease, with manifestation of involuntary muscular contractions and required general anesthesia for bilateral tonsillectomies. Understanding the presentation and characterization of this unusual disease may be helpful in making choice of anesthetics or anesthetic techniques. Its possible mechanisms of action and its specific considerations in anesthesia in the literature are reviewed and discussed.

Adult↗
PubMedDate not supplied

Congenital myopathy with uniform type 1 fiber predominance and type 2 fiber hypoplasia: report of one case.

A 2-month-old female infant, presented with frequent choking and cyanosis during feeding, and poor sucking capability since the age of 45 days. Growth retardation with body weight and length below the third percentile, and head girth below the tenth percentile, were noted on admission. Generalized hypotonia, mild proximal muscle weakness and diminished tendon reflex were also noted. A biopsy from the left quadriceps femoralis showed uniform type 1 fiber (90%) predominance, and a decrease in fiber size and number of type 2 fibers. A biopsy from her father revealed uniform type 1 predominance (99.8%) and 30% central nuclei change. The course of her illness was rather short, and the patient has developed normally since the age of 4 months. Significant improvement in muscle strength and normal intelligence were observed after 3 years of clinical follow-up.

Female↗
PubMed1998

[A case of fasciitis associated with Basedow's disease and polymyositis].

A 39-year-old female suffered from diffuse goiter, palpitation, finger tremor and body weight loss for about one year. Then she developed acute onset of myalgia and swelling of calves, and muscle weakness of proximal limbs. She could not walk because of myalgia and muscle weakness, and was admitted to our hospital 4 days after the onset of muscle symptoms. On admission, her pulse was 110 per minute and she had finger tremor of 11-12 Hz. The thyroid gland was markedly and diffusely enlarged with an elastic soft surface. She presented muscle weakness of proximal limbs and neck, and had intermittent swelling and myalgia on calves. Deep tendon reflexes were increased in all extremities. The erythrocyte sedimentation rate was 22 mm per hour. Eosinophilia was not recognized. Serum CK level was elevated to 671 IU/l. Serum free T3 was higher than 21.7 pg/ml and free T4 was also elevated to 10.19 ng /dl. Serum TSH was lower than 0.05 microU/ml and thyroid stimulating antibody was 1,302.0%. Muscle biopsy of her left gastrocnemius muscle revealed markedly hypertrophic fascia with inflammatory cellular infiltration on HE staining. Inflammatory change was also recognized in muscle tissue and in perivascular region of perimysium. Variation of fiber size, necrotic fibers, and central nuclei were also seen. From these clinical and laboratory findings she was diagnosed as having Basedow's disease associated with fasciitis and polymyositis. Her thyroid function was improved by anti-thyroid drug, and swelling and myalgia of sural regions and weakness of proximal limbs were also improved by steroid therapy. Only one case of Basedow's disease associated with fasciitis and seven cases of that associated polymyositis have so far been reported. This is the first case report of fasciitis associated with Basedow's disease and polymyositis.

Adult↗
PubMed1998

[A case of acute multifocal motor neuropathy with conduction block after Campylobacter jejuni enteritis].

The patient was a 25-year-old male with acute multifocal motor neuropathy with conduction block (MMNCB) after Campylobacter jejuni enteritis. After having suffered from diarrhea for 3 days, he rapidly developed asymmetrical distal-dominant muscle weakness in all extremities. Sensory disturbance was unremarkable except for slight disturbance in deep sensation. Deep tendon reflexes were normal throughout the course of present illness. CSF analysis revealed increased protein up to 66 mg/dl without pleocytosis. In electrophysiological examinations, persistant multifocal conduction blocks in the motor nerves were predominantly noted in the distal part of the extremities. Serum titers of anti-Campylobacter jejuni antibody, anti-GM1 antibody and anti-GalNAc-GD1a antibody were elevated. Muscle weakness resolved completely within 7 weeks. The sural nerve biopsy did not reveal either axonal degeneration, nor demyelination. These clinical and laboratory findings suggested that this case was most likely an acute type of MMNCB after Campylobacter jejuni enteritis.

Acute Disease↗
PubMed1998

[Progressive multifocal leukoencephalopathy (PML). Report of a case diagnosed by amplification of JC virus DNA from cerebrospinal fluid (CSF)].

We report a 54-year-old Japanese man who was diagnosed as progressive multifocal leukoencephalopathy (PML). He had been maintained on regular hemodialysis for 10 years. He was admitted to our hospital with chief complaints of visual disturbance and disorientation. On neurological examination, he was somnolent, and showed mild weakness in the right upper and lower limbs. Deep tendon reflexes were brisk on the right upper and bilateral lower limbs. Sensory examination revealed no abnormal findings. The cerebrospinal fluid (CSF) showed five mononuclear cells/mm3, protein 39 mg/dl and glucose 38 mg/dl. Brain MRI revealed multiple hyperintense lesions in T2-images, which were confined to the white matter of bilateral occipital and the left frontal lobes without an enhancement after gadolinium administration. Using polymerase chain reaction, we amplified the JCV regulatory region from the CSF of the patient. The amplified product contained a rearranged regulatory region that could have been generated from the archetype by deletion and amplification. PML was diagnosed on the basis of these findings. The patient died 7 months after onset of the symptoms. The diagnosis of PML was confirmed by the postmortem findings. The present case indicates that PCR of JCV from CSF is very useful for definitive diagnosis of PML.

Brain↗
PubMed1998

[A case of chronic inflammatory demyelinating polyradiculoneuropathy complicated by phrenic nerve palsy].

We report on a patient with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) complicated by phrenic nerve palsy. A 50-year-old man was admitted to our hospital due to dyspnea and numbness in his limbs. On admission, severe muscle atrophy, weakness, and sensory disturbance were seen in the distal part of his extremities. Deep tendon reflexes were absent in all the limbs. Routine blood examinations showed no abnormal findings except for mild hyperglycemia (fasting blood sugar 145 mg/dl). Right phrenic nerve palsy was observed on a chest roentgenogram and % vital capacity (%VC) was 56%. Cerebrospinal fluid showed elevated levels of total protein (116 mg/dl) and IgG (16.9 mg/dl). Sural nerve biopsy revealed severe loss of myelinated fibers with demyelination and onion-bulb formation. After immunoadsorption plasmapheresis, the phrenic nerve palsy improved rapidly and %VC recovered to 76%. Although phrenic nerve palsy is rare in patients with CIDP, it is important to take notice of this condition, because phrenic nerve palsy is critical when it occurs bilaterally or when it develops in patients who have suffered from respiratory diseases. Immunoadsorption plasmapheresis is one of the effective treatments for CIDP, especially in patients with serious complications such as phrenic nerve palsy.

Chronic Disease↗
PubMed1998

[A 45-year-old man with peripheral monocytosis and right hemiparesis].

We report a 45-year-old man with monocytosis and right hemiparesis. The patient suffered from an acute myocardial infarction from which he recovered completely when he was 42 years old. One year prior to his death, he was found to have increase in monocyte count (35.5% of leukocytes) in peripheral blood and splenomegaly; he was admitted to the hematology service of our hospital. He was diagnosed as having chronic myelomonocytic leukemia after bone marrow examination. He was treated with radiation therapy with improvement in splenomegaly. In May of 1995, he had fever, anemia, and thrombocytopenia for which he needed daily blood transfusion. In November of 1995, he had an onset of weakness in his right hand, and neurologic consultation was asked for in November 27, 1995. Neurologic examination revealed a chronically ill japanese man in no acute distress. He was alert and not demented. Higher cerebral functions were intact. Cranial nerve examination revealed right facial paresis of the central type. Motor-wise, he was right hemiparetic. Generalized muscle wasting was noted apparently due to the chronic debilitating disease. Deep tendon reflexes were within normal range in the right upper extremity, but were diminished in other areas. Sensation was intact, and no meningeal signs were noted. Pertinent laboratory findings were as follows: Hb 8 g/dl, RBC 238 x 10(4)/microliter, WBC 2,900/microliter (band 1.0%, seg 18.5%, lym 28.0%, mono 44.0%, Baso 2.5%), Plt 13 x 10(4)/microliter, PT 16.6"/10.9", APTT 44.7"/35.0". CSF contained 87 mg/dl of protein, 155 mg/dl of glucose and 2 mononuclear cells/microliter. Bone marrow was slightly hypercellular with mild increase in blast forms. No chromosome abnormality was found. CT and MRI revealed a large mass in the left fronto-parietal region and the meninges showed marked thickening with enhancement after gadolinium-DTPA in MRI. The patient was treated with glycerol and steroid, but the subsequent course was complicated by a seizure, agitation, and pneumonia. He died from respiratory failure on January 13, 1996. The patient was discussed in a neurologic CPC and the chief discussant arrived at the conclusion that the patient had chronic myelomonocytic leukemia with infiltration of leukemic cells into meninges and the parenchyme of the cerebrum. Thickening of the dura was thought to be in part a reaction to the subdural hematoma as well as to leukemic cells along the meninges. Postmortem examination revealed hypercellular bone marrow with increase in monocytic cells (more than 20%). The lungs showed pneumonia with scattered old tuberculous lesions. The heart showed an old myocardial infarction in the posterior wall of the left ventricle. The brain showed an old chronic subdural hematoma in the left fronto-temporal region and a cystic mass lesion in the left frontoparietal region. The mass was hypercellular and most of them were monocytes. The dura mater showed reactive thickening without leukemic cell infiltration. It was concluded that this patient had chronic myelomonocytic leukemia with a formation of leukemic mass in the brain. Pathologists thought that the mass was a hematogenous spread. It is rare for chronic myelomonocytic leukemia to form a mass lesion in the brain.

Brain↗
PubMed1998

The effectiveness of intermittent hyperbaric oxygen in relieving drug-induced HIV-associated neuropathy.

This 3-month study evaluated the effects of hyperbaric oxygen on drug-induced neuropathies in 22 patients with human immunodeficiency virus. All patients included in the study had been taking an antiretroviral medication for at least 12 months and had subjective symptoms of numbness or tingling, lethargy, and a decrease in deep tendon reflex. Patients with an active substance abuse history or Kaposi's sarcoma were excluded. Of the 20 patients who completed the series, 17 had significant improvement, 2 had a demyelinating disorder that may have affected the outcome, and 1 had no change.

Anti-HIV Agents↗
PubMed1998

[X-chromosomal bulbospinal muscular atrophy (Kennedy syndrome)].

Two brothers with slowly progressive weakness and congenital nystagmus are presented. DNA analysis confirmed X-linked recessive bulbospinal muscular atrophy (XBSMA, Kennedy's disease) by demonstration of increased size of a CAG-triplet repeat on the androgen receptor gene on the X-chromosome. XBSMA is characterized by almost symmetrical muscular atrophy, weakness and fasciculations predominantly of bulbar, facial and proximal muscles of the extremities, with onset in the third to fifth decade. Tendon reflexes are depressed and pyramidal signs are absent. Sensory symptoms are clinically rare, but sensory nerve action potentials are frequently abnormal. Additional symptoms are important for differential diagnosis, and include postural tremor, gynecomastia, diabetes mellitus, testicular atrophy and impotence. Differentiation of this hereditary disorder from treatable conditions such as multifocal motor neuropathy or amyotrophic lateral sclerosis is essential. Though life expectancy is normal, patients become disabled in the course of the disease and need supportive care. Periodic testing for diabetes is recommended, and genetic counseling should be provided for patients and their relatives.

Adult↗
PubMed1997

[Peripheral neuropathy caused by thallium poisoning].

A 20-year-old man developed over three weeks a sensory and painful neuropathy associated with diffuse alopecia. There was motor weakness, and superficial and deep hypoesthesia of the inferior limbs. Deep tendon reflexes were normal. Electrophysiological study mainly showed axonal motor neuropathy. This patient was admitted six weeks after the first symptoms. The clinical picture suggested thallium poisoning, which was confirmed by thallium concentrations in plasma, urine, hair and nails. After search, thallium was identified in a rat poison.

Adult↗
PubMed1998

Subacute multifocal painful neuropathy with spontaneous remission.

We present the cases of two patients with subacute onset of multifocal painful neuropathy with spontaneous remission and no relapse. The distribution of pain in patient 1 was hands (median > ulnar nerve region) and feet (peroneal and terminal tibial nerve regions), and in patient 2, hands (ulnar nerve region) and feet, left worse than in right. Both patients experienced facial numbness. Deep tendon reflexes were intact except for absent ankle jerks in patient 2. Motor nerve conduction studies demonstrated a marked prolongation of the distal motor latencies with normal proximal segment conduction velocities, suggesting distal demyelination. Cerebrospinal fluid protein concentration was elevated in patient 2, but no definite abnormality was found on sural nerve biopsy. A demyelinating neuropathy with a monophasic self-limited course may be consistent with Guillain-Barre syndrome (GBS). However, the multifocal painful sensory symptoms with facial numbness and the marked distal nerve conduction slowing in our cases are not consistent with GBS.

Adult↗
PubMed1998

[Paraneoplastic neuropathy with positive anti-Hu].

The case of a 72-year-old woman presenting sensory neuropathy and anti-Hu antibodies is reported. She was admitted in November 1995 with a one year history of sensory neuropathy. Her first symptoms were painful numbness and dysesthesias in both feet. She experienced progression of the sensory symptoms affecting upper limbs, and clumsiness of gait. One month before admission she complained of diminished strength in both hands. The neurologic examination showed anicocoric fixed pupils, with no reaction to light; convergence miosis was evident in the right eye (Argyll-Robertson pupil). In the lower limbs she had very mild distal weakness, and tendon reflexes were universally abolished. Pin and touch sensation, position sense and pallesthesia were absent in all four limbs. Romberg test was elicited, and a tabetic gait was patent. Pseudoathetotic movements were observed in hands and feet. An ulcer was present in the fifth finger of the right foot. Routine blood biochemistry and hematology showed a ESR of 105 and an increased IgG in the immune-electrophoretic run. Neurophysiologic evaluation disclosed a mild demyelinating neuropathy. Positive anti-Hu antibodies were found in the serum (Western blot - Athena Diagnostics); CSF was normal but not tested for anit-Hu. An abdominal CT scan disclosed multiple hypodense nodules in liver, right adrenal gland and peritoneum. A chest CT scan showed a hyperdense mass in the lower right pulmonary lobe and enlarged retrocava-pretracheal lymph nodes. A biopsy of the peritoneal nodule was performed, showing a metastatic small cell carcinoma. The patient died eight days after discharge. Although multiple organs were affected, she was independent until death, showing an indolent clinical course.

Aged↗
PubMed1998

[Steroid therapy and plasmapheresis in chronic inflammatory demyelinating polyradiculoneuropathy: a long-term follow-up study].

We report eight patients with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), paying special attention to the therapeutic effects of steroid and plasmapheresis. Each patient underwent 4 to 51 plasmapheresis sessions in addition to prednisolone therapy. Plasmapheresis was more effective in patients with motor neuropathy (6 patients) than in those with sensory neuropathy (2 patients). Concomitant steroid therapy enhanced the short-term efficacy of plasmapheresis. During a long-term follow-up, the patients who showed deteriorating clinical symptoms such as limb weakness, sensory disorder, decreased deep tendon reflexes and increased CSF proteins underwent plasmapheresis once or twice a month. This intermittent plasmapheresis could reduce the use of prednisolone or eventually discontinue the drug completely. We were not able to determine whether immunoadsorption plasmapheresis or double-filtration plasmapheresis was more effective for the patients with CIDP. CIDP is characterized by frequent recurrences of a chronic progressive course, and peripheral neuropathy and some patients with this disease are resistant to many therapeutic approaches. The present study strongly suggests that plasmapheresis with concomitant steroid therapy is very useful for both short- and long-term treatment of CIDP patients.

Administration, Oral↗
PubMed1998

[Ataxic form of Guillain-Barré syndrome associated with acute hepatitis A--a case report].

A 46-year-old male developed a fever of 38 degrees C and general fatigue, and two days later dysesthesia of limbs and muscle weakness of upper extremities appeared. He had difficulty in walking because of truncal and limb titubation and was admitted to our hospital. On admission, pin-prick and soft-touch sensation was reduced in the distal portion of all four extremities, and mild muscle weakness of limbs was noted. He also presented marked disturbance of vibratory and position sense, and had sensory ataxia. All deep tendon reflexes were absent. Moderate liver dysfunction was noted and serum IgM-HA antibody was positive. CSF total protein was elevated to 123 mg/dl on admission. Motor conduction velocity was mildly delayed in the lower extremities, and sensory conduction velocity was mildly delayed in the ulnar nerves and the left sural nerve. The serum of the patient had low titer of IgG anti-sulfated glucuronyl paragloboside (SGPG) antibody. The biopsy specimen from his right quadriceps femoris muscle showed subsarcolemmal aggregates of abnormally enlarged mitochondria with paracrystalline inclusions by electron microscopy. After admission neurological symptoms worsened. Severe diturbance of deep sensation and severe sensory ataxia persisted for a month and slowly improved thereafter. CSF total protein was elevated up to 760 mg/dl. He was treated with plasmapheresis of 12 times and was discharged on the 176th day after the onset, but he could not still walk by himself at that time. Diturbance of deep sensation still remained for one and a half years after the onset. Guillain-Barré syndrome (GBS) associated with acute hepatitis A is rare. In addition, there have been no previous reports describing abnormal mitochondrial changes of the skeletal muscle in GBS.

Acute Disease↗
PubMed1998

[A patient with focal bi-parietal atrophy presenting motor clumsiness and cortical sensory loss].

We report a 73-year-old woman who presented progressive motor clumsiness, cortical sensory loss, and focal parietal lobe atrophy. She was well until one year prior to the present admission when she suffered from what appeared to be mild Fisher syndrome from which she showed excellent recovery. However, soon she noted a gradual onset of difficulty in hand movements and in the recognition of objects by hands. Neurologic examination revealed an alert and well oriented Japanese woman without dementia. Cranial nerves were unremarkable. Although, she did not have aphasia, apraxia, or agnosia, she showed marked clumsiness in skilled hand movements such as using chopsticks, hand writing, and buttoning. She had no motor weakness, ataxia, rigidity, or spasticity. Deep tendon reflexes were symmetrically diminished. Sensory examination revealed cortical sensory loss such as disturbances of two point discrimination, weight sensation, and stereotactic sensations. Her motor clumsiness appeared to be caused by her cortical sensory loss. MRI revealed marked focal atrophy in the bilateral parietal lobe, particularly in the postcentral gyrus and the adjacent association areas. Recently, neurodegenerative disorders with focal brain atrophy such as corticobasal degeneration, Pick's disease, and dementia of frontal lobe type have been reported, however, our patient does not fit to any of these known disorders nor clinical features are distinctly different from Alzheimer's disease. Our patient may be another example of progressive cerebral degeneration with emphasis on the parietal cortex.

Aged↗