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PubMed1995

"Pure" striatonigral degeneration and Parkinson's disease: a comparative clinical study.

Striatonigral degeneration (SND) is difficult to diagnose in vivo. The purpose of this study was to detect the best indicators for an early and reliable diagnosis of the disease. Eighteen patients clinically diagnosed as having SND were selected with rigorous inclusion criteria and compared to 18 patients with Parkinson's disease (PD) matched for age and disease duration. Apart from dysautonomia, the principal discriminant clinical features that distinguished SND from PD were the early appearance of the following symptoms and signs: (a) severe and atypical progressive parkinsonism characterized by bilateral bradykinesia and rigidity, slowness of gait, postural instability, and falls, and poor or absent response to adequate levodopa treatment; (b) increased tendon reflexes associated or not with frank pyramidal signs, severe dysarthria, and less consistently, dysphagia, stridor, antecollis, and stimulus-sensitive myoclonus, which, when present, are highly suggestive of the disease.

Aged↗
PubMed1998

Progressive pseudobulbar paresis, early choreiform movements, and later rigidity: appearance in two sets of dizygotic twins in the same family.

In a family with two sets of dizygotic twins, three, possibly all four, siblings were affected by the same disorder. The parents were unrelated and the illness seemed limited to one generation. Onset was in the early to mid-20s with tics and choreiform movements, dysarthria, and dysphagia. Two twins had epilepsy. There was a marked dyscoordination of bulbar musculature reminiscent of pseudobulbar paresis. Involuntary movements were prominent during the first years, but then disappeared and were replaced by an akinetic-rigid parkinsonian appearance in the late stage. The intellect remained largely intact. Tendon reflexes were reduced. Varying degrees of peripheral nerve changes were seen. Two patients died after 22-24 years from causes indirectly related to the main illness. Marked degenerative changes were found in the caudate nucleus and putamen. Acanthocytes in significant numbers could not be detected in peripheral blood. Lipoproteinelectrophoresis was normal. Creatine kinase levels were moderately raised in one patient, normal in the others. Although certain clinical resemblances exist with neuroacanthocytosis, the exact nosologic status of the disorder has not been determined.

Adult↗
PubMed2001

Motor nervous pathway function is impaired after treatment of childhood acute lymphoblastic leukemia: a study with motor evoked potentials.

BACKGROUND: The objective was to evaluate whether motor nervous pathways are affected when patients are treated for childhood acute lymphoblastic leukemia (ALL). PROCEDURE: Thirty-two children with ALL were studied at the end of treatment by means of motor evoked potentials (MEPs) elicited by magnetic stimulation (MS) transcranially and peripherally and underwent a detailed neurological examination. Thirty-two healthy children matched with them for age, sex, and height served as a control group. RESULTS: The latencies of the MEPs were significantly prolonged along the entire motor nervous pathway in the patients with ALL compared with the healthy controls, indicating demyelination in the thick motor fibres. The MEP amplitudes of the distal extremities elicited by stimulation at the brachial plexus and LV spinal level were significantly lowered in the patients treated for ALL, also indicating anatomical or functional loss of descending motor fibres and/or muscle fibres. The MEP amplitudes elicited by cortical MS showed wider variation and no clear abnormalities were found. Neurological signs and symptoms were common after treatment: 41% of the patients had depressed deep tendon reflexes, 31% had fine motor difficulties and 63% gross motor difficulties, and 34% had dysdiadochokinesia. The conduction delay within the peripheral nerve was related to the post-therapeutic interval after administration of vincristine and the lesions within the CNS to the number of injections of intrathecal methotrexate. CONCLUSIONS: The present results show adverse effects of the ALL treatment on the entire motor nervous pathways. In our experience, the measurement of MEPs by MS provides an objective, painless, and practical tool for assessing the treatment-related neurotoxicity in both the CNS and the peripheral nerves. These disturbances in the motor nervous pathways at the end of treatment raise the question of the long-term effects of ALL treatment on the motor nerve tracts, and have led us to employ MEPs to study these effects in long-term survivors of ALL.

Adolescent↗
PubMed2003

Depression of spinal motoneurons may underlie weakness associated with severe anemia.

A 37-year-old woman had a 2-week history of progressive weakness, muscle hypotonia, and absent or hypoactive deep tendon reflexes. Nerve conduction studies showed diminished H-reflexes and absent or decreased persistence of F-waves in all limbs. The patient was admitted to the hospital with a diagnosis of Guillain-Barré syndrome. Laboratory studies revealed severe anemia with a hemoglobin level of 4.1 g/dl and hematocrit of 15.1%. Immediate blood transfusion resulted in a hemoglobin of 13.2 g/dl and hematocrit of 40.2%, associated with rapid neurological recovery (normal stretch reflexes and muscle strength) and normalization of F-waves and H-reflexes. This case demonstrates that severe anemia may be associated with signs and symptoms that mimic Guillain-Barré syndrome, both clinically and electrophysiologically. It also suggests that a relative depression of spinal motoneuron excitability may be a possible mechanism for the weakness that is commonly observed in severe anemia.

Adult↗
PubMed2003

Compressive lumbar myelopathy presenting as segmental motor neuron disease.

Four patients presented with slowly progressive, bilateral, asymmetric weakness and muscle atrophy in the lower extremities, accompanied by cramps and fasciculations. Sensory symptoms were insignificant. There was no bladder or bowel disturbance. Upper extremities and cranial nerves were normal. Weakness was found in lumbosacral myotomes, ranging from L2 to S1. The tendon reflexes varied, and extensor plantar responses were found in one case with proximal leg involvement. Nerve conduction studies were normal, but segmental chronic and often active denervation confined to the weak myotomes in the lower extremities was found in the electromyogram. Magnetic resonance imaging showed evidence of spondylotic lumbosacral myelopathy associated with disc herniation or osteophytic arthropathy at the T11/T12 spinal level in all patients, with increased signal within the adjacent cord. This unusual purely motor presentation may result from ischemic myelopathy secondary to compression of the anterior spinal artery.

Adult↗
PubMed2003

Peripheral neuropathy in scleroderma.

Because patients with scleroderma report neuropathic symptoms including numbness, paresthesias, and dysesthesias, we assessed peripheral nerve function in such patients. Fourteen scleroderma patients underwent complete neurologic examination, nerve conduction studies (NCS) and quantitative sensory testing (QST). Neurologic examination revealed reduced vibration (7) or pinprick (4) sensation in the upper or lower extremities, focal atrophy or proximal weakness (2), and decreased deep tendon reflexes (2). NCS showed reduced sensory nerve action potentials (1) and carpal tunnel syndrome (1). QST of the upper and lower extremity revealed increased cold or vibration detection thresholds in 8 of 14 patients. Our findings suggest that peripheral neuropathy occurs in patients with scleroderma at a higher frequency than previously appreciated. These findings cannot be ascribed to compression neuropathies, but rather involve large and small fibers in a non-length-dependent fashion. Larger, prospective studies using the more sensitive QST as well as pathologic studies of nerve, including cutaneous innervation, are needed to further assess the characteristics and etiology of the neuropathy.

Adult↗
PubMed2004

Acute multiple cranial neuropathy: a variant of Guillain-Barré syndrome?

Three patients with acute multiple cranial neuropathy following benign infectious disease are reported. Complete or partial ophthalmoplegia, as well as facial and bulbar dysfunction, were noted in all. Cranial nerve involvement was bilateral. Other neurological deficits included sensory loss in two patients and transiently reduced tendon reflexes in the left arm in one. One patient had positive serum anti-GQ1b immunoglobulin G antibody during the acute phase of the illness. The cerebrospinal fluid had a normal cell count in all three patients, with raised protein concentrations in two. Electrophysiological evaluation showed peripheral nerve dysfunction in two patients. All three patients improved either spontaneously or coincident with immunotherapy. Our patients had many clinical features resembling those of typical Guillain-Barré syndrome (GBS), and hence their disorder may represent a regional variant, that is, a cranial form, of GBS. This form of GBS accounted for 5% of the GBS patient population in our series.

Acute Disease↗
PubMed2006

Clinicopathological phenotype of ALS with a novel G72C SOD1 gene mutation mimicking a myopathy.

A 71-year-old woman with a family history of amyotrophic lateral sclerosis (ALS) was investigated for symmetrical, proximal limb and abdominal muscle weakness. Initial examination showed mild proximal muscle weakness in the arms and legs, slightly elevated serum creatine kinase (CK) level, and normal electromyographic (EMG) findings. A myopathy was the presumed diagnosis. Over the next year, weakness became severe and tendon reflexes became unelicitable; no upper motor signs were present. EMG then showed acute and chronic denervation and a muscle biopsy showed target fibers and grouped atrophy. DNA analysis revealed a G72C CuZn-superoxide dismutase (SOD1) mutation. Fasciculations were absent throughout the disease. The patient died 53 months after symptom onset and autopsy revealed loss of lower motor neurons (LMN) and SOD1-positive inclusions. This case expands the phenotypic spectrum of ALS associated with SOD1 mutations to include presenting features that mimic a myopathy.

Aged↗
PubMed2006

Peripheral neuropathy in an outpatient cohort of patients with Sjögren's syndrome.

Peripheral neuropathy is common in patients with Sjögren's syndrome (SS), but its precise prevalence is unknown. Most prior studies were conducted at neurology or rheumatology specialty clinics and likely selected for a more severely affected population. We evaluated 22 SS patients and 10 controls for evidence of neuropathy in an outpatient setting at a regional meeting of the Sjögren's Syndrome Foundation. We performed neurological examinations and nerve conduction studies (NCSs) and measured serum antinuclear antibody (ANA) and SS-A and SS-B antibody levels. Participants filled out a questionnaire pertaining to symptoms, diagnosis, and treatment. We found that signs and symptoms related to small axons were more common in patients with SS than in controls. Complaints of painful distal paresthesias in the feet were noted in 59% of patients but in only 10% of controls, and of abnormal sweating in 41% and 0%, respectively. Examination revealed decreased pinprick sensation in 64% of patients with SS, but in only 30% of controls. Overall, 45% of the patients but none of the controls were thought to have an isolated small-fiber neuropathy. Large-fiber dysfunction (as measured by testing vibration, deep tendon reflexes, and NCSs) was similar between the two groups. We conclude that small-fiber neuropathy is common in patients with SS.

Antibodies, Antinuclear↗
PubMed2006

Expanding the phenotypes of the Pro56Ser VAPB mutation: proximal SMA with dysautonomia.

The phenotype of 16 members of a family affected by a late-onset, dominant, progressive, motor and autonomic disorder is described. The VAPB (Pro56Ser) mutation was detected in Brazilian families with different phenotypes of motor neuron disorders. In this family, proximal and axial muscle weakness and atrophy, associated with abdominal protrusion, defined the motor phenotype. Death occurred in 10-15 years due to respiratory insufficiency. Tone and tendon reflexes were decreased and a distal tremor was common. Sensation was preserved. Autonomic abnormalities were also present, including choking, chronic intestinal constipation, sexual dysfunction, and sudomotor abnormalities, and on nerve morphology there was involvement of unmyelinated fibers. Electromyography disclosed ongoing denervation and reinnervation. Isolated dysfunction of motor and autonomic neurons is unusual among the spinal muscular atrophies. On this basis, this condition seems to represent a new category of disease.

Adult↗
PubMed2007

Uremic neuropathy: clinical features and new pathophysiological insights.

Neuropathy is a common complication of end-stage kidney disease (ESKD), typically presenting as a distal symmetrical process with greater lower-limb than upper-limb involvement. The condition is of insidious onset, progressing over months. and has been estimated to be present in 60%-100% of patients on dialysis. Neuropathy generally only develops at glomerular filtration rates of less than 12 ml/min. The most frequent clinical features reflect large-fiber involvement, with paresthesias, reduction in deep tendon reflexes, impaired vibration sense, muscle wasting, and weakness. Nerve conduction studies demonstrate findings consistent with a generalized neuropathy of the axonal type. Patients may also develop autonomic features, with postural hypotension, impaired sweating, diarrhea, constipation, or impotence. The development of uremic neuropathy has been related previously to the retention of neurotoxic molecules in the middle molecular range, although this hypothesis lacked formal proof. Studies utilizing novel axonal excitability techniques have recently shed further light on the pathophysiology of this condition. Nerves of uremic patients have been shown to exist in a chronically depolarized state prior to dialysis, with subsequent improvement and normalization of resting membrane potential after dialysis. The degree of depolarization correlates with serum K(+), suggesting that chronic hyperkalemic depolarization plays an important role in the development of nerve dysfunction in ESKD. These recent findings suggest that maintenance of serum K(+) within normal limits between periods of dialysis, rather than simple avoidance of hyperkalemia, is likely to reduce the incidence and severity of uremic neuropathy.

Axons↗
PubMed1995

Facilitation of motor evoked potentials: timing of Jendrassik maneuver effects.

Remote voluntary contraction, such as the classical Jendrassik maneuver (JM), is a procedure routinely used to increase the amplitude of tendon reflexes in the lower limb. In 8 healthy subjects we studied the effects of JM on the motor evoked potentials (MEP) recorded from tibialis anterior muscle, produced by transcranial magnetic stimulation (stimulus output of 5-10% over motor threshold). In this study, JM consisted here of a bilateral violent handgrip, preceding magnetic stimulation from 100 to 50 ms (steps of 100 ms). Compared to the control test, latencies remained unchanged. MEP amplitudes were greatly enhanced with a JM test interval from 200 to 400 ms (170% of control amplitude at 300 ms). We also studied 6 patients with severe alterations of MEPs from tibialis anterior muscle. In each case, JM preceding magnetic stimulation (stimulus output 100%) from 300 ms induced reappearance of response or marked enhancement of amplitude, allowing calculation of central conduction time. Such a technique, which is easy to perform, may be useful in clinical practice to calculate central motor conduction time, where it would otherwise be difficult or impossible.

Adult↗
PubMed2003

Urinary dysfunction in patients with systemic lupus erythematosis.

AIMS: Nervous system involvement occurs in about half of patients with systemic lupus erythematosis (SLE). Seizures and psychiatric disorders are the most common manifestations; spinal cord lesions are uncommon. We had eight such patients who presented with urinary dysfunction. METHODS: The patients consisted of two men and six women, mean age 42 years, range 28-72 years. All patients were suffering from SLE for 2-25 years under immunosuppressant therapy. Their neurological manifestations were subacute encephalomyelopathy in three, subacute myelopathy in one, and chronic myelopathy in four. Urinary dysfunction included voiding difficulty in six (two of them had urinary retention initially) and urinary incontinence in four. Standard urodynamic studies were performed in the patients 2-3 weeks after admission. RESULTS: All patients had urodynamic abnormalities, including decreased urinary flow in five, increased post-void residual urine in three (mean 97 ml), increased maximum urethral closure pressure in two, detrusor hyperreflexia (DH) in five, impaired detrusor contractility in five, detrusor-sphincter dyssynergia in four, and neurogenic motor unit potentials of the external sphincter in two of four patients studied. DH was more common in patients with brisk deep tendon reflex (80%) than in those without (33%). Repeated studies showed that one had loss of bladder sensation, one developed a low compliance bladder, and one had decreased bladder capacity from 470 to 40 ml with marked DH during 2 months to 8 years follow-up period. CONCLUSIONS: Our results suggest that urinary dysfunction can be a feature in SLE patients is most commonly due to, and, in some patients there myelopathy, may be involvement of the spinal cord in a small group of the patients.

Adult↗
PubMed2002

Neurodevelopmental investigations among methylmercury-exposed children in French Guiana.

French Guiana, like its neighbors, suffers from environmental pollution with methylmercury from gold mining activities, and Amerindian communities are particularly affected. A neurological and a neurospsychological evaluation were carried out in children of three Amerindian communities with various levels of pollution: 156 children from the Upper Maroni (high exposure), 69 from Camopi on the Oyapock river (median exposure), and 153 from Awala on the Atlantic coast (low exposure). Exposure to methylmercury was measured by determination of total mercury in the hair of the children and their mothers (geometric mean, 12.7 microg/g in Upper Maroni). No major neurologic signs were observed in the children examined. After adjustment for potential confounders, we found a dose-dependent association between maternal hair mercury level and increased deep tendon reflexes, poorer coordination of the legs, and decreased performance in the Stanford-Binet Copying score, which measures visuospatial organization. In this last test, the frequency of rotation errors was high in the 5-6 years age group and increased with mercury exposure. These associations depended on the sex of child and were stronger among boys. The interpretation of these results is limited mainly by the cross-sectional design of the study. It identifies specific neurological and neuropsychological deficits, in some cases modulated by sex, which are consistent with known targets of mercury neurotoxicity.

Child↗
PubMed2004

Recovery from spinal cord injury--underlying mechanisms and efficacy of rehabilitation.

Patients with an acute complete spinal cord injury (SCI) present a syndrome called "spinal shock". During spinal shock the loss of tendon reflexes and flaccid muscle tone is associated with a low persistence of F-waves and loss of flexor reflexes while H-reflexes are well elicitable. When clinical signs of spasticity become established, the electrophysiological parameters show little change. The divergent course of clinical signs of spasticity in their possible neuronal correlates indicate the occurrence of non-neuronal changes contributing to spasticity. - When signs of spinal shock had disappeared in patients with incomplete and complete paraplegia a locomotor pattern can be induced and trained under conditions of body unlaoding using a moving treadmill. In complete and incomplete paraplegic patients an increase of gastrocnemius electromyographic activity occurs during the stance phase of a step cycle with a daily locomotor training, coincident with a significant decrease of body unloading. In contrast to this, neither clinical nor electrophysiological examination scores improve. The locomotor pattern depends on the level of lesion: the higher the level of spinal cord lesion the more 'normal' is the locomotor pattern. This suggests that neuronal circuits underlying 'locomotor pattern generation' in man is not restricted to any specific level of the spinal cord, but extends from thoraco-lumbal to cervical levels.

Animals↗
PubMed1991

The epidemiology of headache among children with brain tumor. Headache in children with brain tumors. The Childhood Brain Tumor Consortium.

In this report we present aspects of the epidemiology of headache (i.e., pain in the head, face, ear, or neck) among children with brain tumors. The data are derived from the 3,291 subjects in the Childhood Brain Tumor Consortium databank. Overall, 62% of the children with brain tumors experienced chronic or frequent headaches prior to their first hospitalization: 58% of children with supratentorial tumors and 70% of children with infratentorial tumors. The relative frequency of headache increased through age 7 and then leveled off regardless of tumor location. For children under age 5, headache rarely had a duration of more than 1 year prior to hospitalization. Among children over age 4, headache duration of at least one year was significantly greater for supratentorial than for infratentorial tumors. Children with a brain tumor and headache had a different distribution of symptoms and neurologic signs than those without headache. Tumor location and headache status were interactively associated with the presence of other symptoms and neurologic signs. Children with headache had a greater number of other symptoms and neurologic signs. Regardless of tumor location among children with headache, nausea or vomiting, papilledema, and hypoactive tendon reflexes were more frequent, while upper extremity weakness, optic atrophy, and irritability were less frequent. Diplopia, coma, stiff neck, anesthesia or hypesthesia, pupillary abnormalities, and abnormalities of personality, academic performance, or speech were associated with headache in children with supratentorial tumors. No specific symptoms or neurologic signs were associated with headache in children with infratentorial tumors. Supratentorial craniopharyngioma, ependymoma, and protoplasmic astrocytoma were associated with significantly high rates of headache as was infratentorial pilocytic astrocytoma.

Adolescent↗
PubMed1985

Acute encephalopathy associated with continuous vincristine sulfate combination therapy: case report.

Neurotoxicity is a well-recognized and commonly observed side effect associated with the use of vincristine sulfate in cancer chemotherapy. The clinical manifestations of vincristine neuropathy cover a wide spectrum of peripheral neurologic dysfunctions that have been described to be reversible and cumulative in most instances (1, 2). Paresthesias, loss of tendon reflexes, and progressive weakness are the most common clinical features (3, 4). Sensory impairment, cranial nerve palsies, gastrointestinal disturbances, and autonomic dysfunctions including atonic bladder, impotence, and orthostatic hypotension may occur (5). Acute CNS complications, usually presenting as generalized seizures, are extremely rare and only a few cases have been reported which were without underlying biochemical or structural abnormalities (1, 5-9). We describe the case of a woman with multiple myeloma, who developed fulminant encephalopathy following 4 days of continuous vincristine, adriamycin, and day 1-4 pulse dexamethasone (VAD) combination therapy.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1993

Inclusion body myositis: clinical and histopathological features of 36 patients.

Thirty-six patients (15 females, 21 males) with inclusion body myositis (IBM) were studied. The diagnosis was established according to clinical and histopathological criteria. Clinical features were insidious onset of slowly progressive muscle weakness and wasting with depressed or absent tendon reflexes especially in the lower limbs. The pattern of muscle weakness was variable. The majority of patients (58%) showed proximal and symmetrical weakness usually most prominent in the legs. Isolated distal (6%) and asymmetrical weakness (19%) was less frequently observed. Myalgia occurred in 42% of the patients. The age at onset of symptoms ranged from 20 to 73 years (mean 47 years). Serum creatine kinase levels were normal (11%) or mildly elevated (89%). Needle electromyography revealed myopathic features in about 80% of the patients, and results of nerve conduction studies were normal in most of the cases. The predominant histopathological findings were numerous muscle fibers with rimmed vacuoles (100% of the patients), groups of atrophic fibers (92%), and inflammatory infiltrates (89%). The inflammatory infiltrates were located predominantly at endomysial sites and were composed mainly of T8 cells. Electron microscopy showed characteristic intracytoplasmic filamentous inclusions in all 36 cases. Immunosuppressive treatment in 16 patients failed to prevent disease progression in all but one patient with an associated Sjögren's syndrome. It is concluded that the consistent combination of typical histopathological findings and characteristic clinical features offers a firm basis for the diagnosis of IBM. IBM should be suspected in any adult patient presenting with clinical signs of a chronic polymyositis unresponsive to immunosuppressive therapy. The etiology and pathogenesis of IBM remain to be established.

Adult↗