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PubMed2001

[Spinal meningioma as differential diagnosis of diabetic polyneuropathy].

HISTORY AND ADMISSION FINDINGS: A 70 year old woman had suffered from diabetes mellitus type 2 since she was 52. Three years before the surgery she had begun to experience weakness together with altered sensitivity in the right leg, which was regarded as having been caused by diabetic polyneuropathy. During the admission examination the level for algesia on the right-hand side was at about D 11, a distal paraparesis of the leg (3-4 degrees, Janda's classification), more intense on the right, hyperactive deep tendon reflexes, Babinski's reflex on both sides, and depressed abdominal cutaneous reflexes. The sensitivity to vibrations on the Malleolus medialis on both sides was 0/8. The patient could walk only with the help of a Rollator. INVESTIGATIONS: Over the three-year period following onset of symptoms the following tests were carried out: motor nerve conduction speeds of the N. tibialis and N. peronaeus, electromyogram of the N. tibialis anterior and the M. gastrocnemius, somatosensory evoked potentials (SSEP) of the N. tibialis, which indicated a lesion in the peripheral nerves or nerve roots. Cranial computed tomography (CCT), CT scan of the lumbar spine (L3-S1) and angiological investigation elicited no significant pathological findings. An MRI of the thoracal spine showed a vertebra-sized dorsal tumor pressing on the spinal cord from left to right. TREATMENT AND COURSE: By means of microsurgery the spinal tumor was completely removed. Suspected meningeoma was confirmed by histological analysis. During the post-surgical period, the incomplete paraplegia quickly regressed, and 7 weeks after the removal of the spinal meningeoma the patient was able to climb stairs. CONCLUSION: In case of slowly-developing paresis of the legs in diabetic patients, diabetic polyneuropathy should not be diagnosed without careful consideration, and rare spinal tumors should be considered as part of the differential diagnosis, especially if the blood glucose level is normal, and intensive physiotherapy brings no improvement in the patient's condition.

Aged↗
PubMed2001

[Fatal brain edema after ingestion of ecstasy and benzylpiperazine].

HISTORY AND ADMISSION FINDINGS: A 23-year-old woman was hospitalized with headache, malaise and somnolence 11 hours after ingestion of A2 (benzylpiperazine), 7 hours after ingestion of ecstasy (MDMA), and large volume of fluids. On admission she had bradycardia (heart rate 48/min), hypertension (blood pressure 154/95 mm Hg), and reduced consciousness with diminished tendon reflexes and non-reacting pupils (Glasgow Coma Score 6). INVESTIGATIONS: Serum sodium was markedly decreased (115 mmol/l [normal 135-145]) with low plasma osmolality (246 mosm/kg [normal 280-300]). Other laboratory findings were within normal limits. TREATMENT AND COURSE: The patient had severe hypervolaemic hypotonic hyponatraemia. 40 minutes after admission she seized twice and was intubated. Brain CT scan showed massive cerebral oedema with beginning tonsillar herniation. Serum sodium concentration returned to normal within 38 hours, but the patient deteriorated neurologically with increasing tonsillar herniation detected in a second brain CT scan. The patient died 57 hours after admission. CONCLUSION: 13 cases of MDMA-associated severe hyponatraemia are reported. Intake of fluids after MDMA ingestion may lead to potentially fatal hypervolaemic hypotonic hyponatraemia with cerebral oedema. Symptoms appear about 8 hours (range 4-18) after MDMA ingestion. Even low doses of MDMA and fluids may lead to a serious outcome. The only risk factor is female gender. Measurement of serum sodium and brain CT scan is recommended in all patients with altered mental status after MDMA consumption.

Adult↗
PubMed2002

Polyradiculoneuritis with myelitis: a rare differential diagnosis of Guillain-Barré syndrome.

AIM: To describe the symptoms, signs, findings and prognosis in children suffering simultaneously from polyradiculoneuritis and myelitis. METHODS: Retrospective review of eight patients aged 2 to 13 years out of 210 patients with polyradiculoneuritis reported from 70 hospitals. Diagnostic criteria for polyradiculoneuritis were: flaccid paresis with loss of tendon reflexes, increased CSF protein and slowing of nerve conduction velocity. Criteria for myelitis were: severe and persistent bladder dysfunction, a sharply defined sensory level and/or evolving spastic paresis, with or without myelitic changes in spinal MRI. RESULTS: In the disease's earliest stage it was difficult to differentiate polyradiculoneuritis with myelitis from classical GBS. However, onset was often unusually rapid compared to GBS. Five patients developed a sensory level and seven suffered from severe bladder dysfunction. Four of the six children studied showed focal myelitic changes in MRI. All seven children with sufficient follow-up remained with residual paresis and significant long-term motor deficits. CONCLUSION: Due to its severe long-term prognosis, polyradiculoneuritis with myelitis must be differentiated from classical GBS. In the disease's early stage, the detection of a sensory level, severe bladder dysfunction and an unusually rapid onset can be helpful. The effect of high-dose corticosteroids is not yet clear. After the acute phase, most children require extended rehabilitation.

Adolescent↗
PubMed2003

X-linked centronuclear myopathy.

We report the cases of two male preterm newborns with X-linked centronuclear myopathy (CNM). This is the most severe type of CNM. Each of them presented with generalized hypotonia, weakness, difficulty in swallowing, and respiratory distress at birth. Physical examination of both newborns revealed long thin face, high-arched palate, mild bilateral ptosis, frog-leg posture, and absence of deep tendon reflex. Diagnosis of the disease was made according to fetal history, family history, muscle histopathology, electron microscopy, and genetic analysis. Subdural hemorrhage of brain and subcapsular hematoma of the liver were found at autopsy of Case 1. The results of molecular analysis of Case 2 and his family favored the diagnosis of X-linked CNM. Molecular studies can be easily performed with only minute amount of DNA of patients, and may help the clinician to predict which patients may be at the risk for medical complications.

Fatal Outcome↗
PubMed2004

Short-chain acyl-CoA dehydrogenase deficiency associated with early onset severe axonal neuropathy.

Two unusual cases of axonal neuropathy associated with short-chain acyl-CoA dehydrogenase (SCAD) deficiency are described. These two unrelated infants presented with profound generalised weakness, particularly affecting the upper limbs. Clinical examination revealed generalised peripheral hypotonia and weakness, with absent deep tendon reflexes. An axonal polyneuropathy was confirmed on electromyogram (EMG) and nerve conduction studies (NCS) and, following an extensive metabolic screen, an acylcarnitine and organic acid profile consistent with a short-chain fatty acid beta-oxidation defect was found. In both cases, SCAD deficiency was confirmed by enzyme analysis. Genetic analysis showed the presence of common gene variations in the SCAD gene. SCAD deficiency is a rare disorder with a wide clinical phenotype. SCAD deficiency associated with axonal neuropathy has not previously been reported. As highlighted in these cases, it may be necessary to include axonal neuropathy as a presenting feature of SCAD.

Age of Onset↗
PubMed2004

Lambert-Eaton myasthenic syndrome.

Lambert-Eaton myasthenic syndrome (LEMS) is an idiopathic or paraneoplastic syndrome producing antibodies against presynaptic voltage-gated P/Q calcium channels. This decreases calcium entry into the presynaptic terminal, which prevents binding of vesicles to the presynaptic membrane and acetylcholine release. LEMS is most often associated with small cell lung cancer, although idiopathic presentations comprise approximately 40% of the cases. The most common initial complaint is proximal muscle weakness involving the lower extremities more than the upper extremities. Depressed deep tendon reflexes and autonomic dysfunction are frequently present. Involvement of the bulbar or respiratory muscles is rare. Diagnosis is confirmed by electrophysiological testing, which demonstrates small compound muscle action potentials and facilitation with exercise or 20-Hz repetitive stimulation. A serum test for voltage-gated calcium channel antibodies is commercially available. Treatment involves removing the cancer associated with the disease. If cancer is not found, immunosuppressive medications and acetylcholinesterase inhibitors are used with moderate success. Patients with idiopathic LEMS should be screened every 6 months with chest imaging for cancer.

Humans↗
PubMed2004

Tick paralysis.

Tick paralysis results from inoculation of a toxin from tick salivary glands during a blood meal. It is a relatively uncommon neuromuscular disease with a higher prevalence among young girls, although older men who get exposed to ticks may also be affected. It typically presents as an acute ascending paralysis occurring a few days after tick attachment and may result in respiratory failure and death. Patients may report minor sensory symptoms but constitutional signs are usually absent. Deep tendon reflexes are usually hypoactive or absent and ophthalmoplegia and bulbar palsy can occur. Children may be ataxic. Electromyographic studies usually show a variable reduction in the amplitude of compound muscle action potentials but no abnormalities of repetitive nerve stimulation studies. These appear to result from a failure of acetylcholine release at the motor nerve terminal level. There may be subtle abnormalities of motor nerve conduction velocity and sensory action potentials. Removal of the tick results in the very rapid reversal of clinical and physiologic deficits, quicker with North American ticks than with the Ixodes species seen in Australia.

Action Potentials↗
PubMed2005

Acute motor and sensory axonal neuropathy (AMSAN) in a 15-year-old boy presenting with severe pain and distal muscle weakness.

Acute motor and sensory axonal neuropathy (AMSAN) is a recently described subtype of Guillain-Barré syndrome characterized by acute onset of distal weakness, loss of deep tendon reflexes and sensory symptoms. Electrophysiological studies show mildly reduced nerve conduction velocities combined with a marked reduction of muscle action and sensory nerve action potentials. Here, we report a 15-year-old boy who suffered from severe burning and knife-like pain that increased over a period of three months and resulted in a disrupted sleep pattern and suicidal intentions as well as marked loss of weight. In addition, he developed muscle weakness in his hands and feet. Neurophysiological and histopathological studies revealed AMSAN. Marked improvement of his condition was achieved by treatment with intravenous immunoglobulins, high-dose methylprednisolone, and a combination of gabapentin, antidepressants, and an oral morphine.

Adolescent↗
PubMed1986

[Differential diagnosis, pathogenesis and therapy of alcoholic polyneuropathy].

The most common forms of polyneuropathies are the alcoholic and diabetic polyneuropathies. They each constitute 1/3 of all polyneuropathies. The first symptoms shown by the alcoholic polyneuropathy are symmetric sensory disturbances with loss of tendon reflexes and of vibration sense in the peripheral segments of the lower extremities. At the beginning one almost always finds pressure pain in the calves. Important differential clues in diagnosis compared to the diabetic neuropathy, are the age at which the disease begins, the degree to which the autonomic nerve fibres and the cranial nerves are affected, as well as the form of manifestation. Pathogenetically, a direct toxic alcohol effect can above all be suspected in accordance with the typical electrodiagnostic findings with a neurogenic pattern in the EMG in the case of normal or slightly diminished conduction velocity, and in agreement with the morphological finding of an axonal degeneration in most of the biopsies. Possibly, in a small number of cases a vitamin deficiency or a malabsorption can play a causal role. The prognosis is good by complete abstinence from alcohol.

Alcoholism↗
PubMed1999

Clinical and genetic correlate in childhood onset Friedreich ataxia.

We analyzed the clinical and genetic aspects of 28 FRDA patients from 20 families. 19 families were consanguineous. The onset was between 4 and 13 1/2 years of age (mean 15.4 +/- 6.2). Three patients presented with cardiomyopathy, one with weakness, and the rest with ataxia. There were two patients with preserved lower-limb deep tendon reflexes. Sensory nerve action potentials were reduced in 14/14 patients. Cardiac echograms were abnormal in 17/19 cases, and this was between 6 and 16 years of age (mean 10.1 +/- 3.5). Four families were multiplex. Clinical intra-familial variability was observed. Increased GAA repeats of the X25 gene were found in 27/28 patients studied, all in a homozygous state. 88.9% of patients had a smaller allele larger than 500 repeats, and 66.7% had more than 700 repeats. The patient who did not have increased GAA repeats in both alleles had peculiar findings. Significant correlation of expansion was obtained for the early onset, and cardiomyopathy as the onset.

Action Potentials↗
PubMed1996

The central nervous system in Tay syndrome.

Trichothiodystrophy (brittle sulfur-deficient hair) is a marker for several autosomal recessive neurocutaneous syndromes with neurological manifestations and mental retardation. In Tay syndrome, the trichothiodystrophy is accompanied by congenital ichthyosis, short stature, delayed physical and mental development and pyramidal tract signs with increase in muscular tone and brisk tendon reflexes. The pathogenesis of these neurological manifestations is not fully elucidated. We present a case of Tay syndrome in which a cranial MRI revealed an almost total lack of myelin within the cerebral hemispheres and a patchy hypomyelination of the cerebellum. In accordance, a strongly prolonged visual evoked response pointed to a dysfunction of the white matter in Tay syndrome.

Ataxia↗
PubMed1995

Primary hypogonadism in females with infantile onset spinocerebellar ataxia.

We recently described an infantile onset spinocerebellar ataxia (IOSCA) in 19 Finnish patients. The classification of hereditary ataxias of unknown etiology is difficult because of the heterogeneity of these diseases. The clinical course of IOSCA is homogeneous. Ataxia, muscle hypotonia, athetosis, and loss of deep tendon reflexes in the legs appeared around the age of 1 year. Ophthalmoplegia and deafness were found by school-age, and sensory axonal neuropathy and optic atrophy by adolescence. An acute crisis with epilepsy was a late manifestation. The female patients had hypogonadism. In order to define the type of hypogonadism and to exclude other endocrine defects we measured serum concentrations of SHBG, DHEAS, prolactine, testosterone/estradiol, FSH and LH in postpubertal patients. ACTH, hCG and GnRH tests were performed to both pre- and postpubertal patients. Growth was analysed, and the brain and pituitary region were examined with magnetic resonance imaging (MRI). The estradiol values were low and FSH and LH values were high in the female patients, which indicates that the hypogonadism was of the hypergonadotropic type. The growth of the female patients was steady without a significant pubertal growth acceleration. The growth and pubertal development of the male patients were normal. The adrenal cortical and thyroidea functions were normal in all patients.

Adolescent↗
PubMed1997

[Status epilepticus late in pregnancy--eclampsia or subarachnoid hemorrhage?].

After a largely inconspicuous pregnancy, a 31-year old primipara suffered from a status epilepticus in the third trimenon. The convulsions could not be terminated by emergency medical services, resulting in aspiration of gastric contents. Assuming eclampsia, an emergency caesarean section was performed immediately in a central hospital. Postoperatively, a pathological pattern of tendon reflexes was noticed. A CT scan revealed subarachnoid haemorrhage. The causal aneurysm of the right A. pericallosa was clipped subsequently. Eclampsia is the leading cause of epileptic seizures during pregnancy. However, a different aetiology should always be considered, especially if medical history does not reveal symptoms of pre-eclampsia.

Adult↗
PubMed1993

[Normal and frequent neurologic findings in elderly patients].

Numerous normal age-related changes that occur in the nervous system differ more quantitatively than qualitatively from certain common neurological diseases of elder individuals. Changes in the cranial nerve examination primarily relate to an age-related decline in sensory functions, especially of vision and hearing, and to a restriction in the range of eye movements, especially vertically. A progressive decline in the bulk and strength of muscles and in the speed and coordination of movements has long been recognised as an accompaniment of aging. Posture and gait show conspicuous changes with advancing age, partially correlating with diminished sensation in the legs and/or with a nonspecific bradykinetic senile gait. The distal depression of deep tendon reflexes and sensory function is primarily due to distal degeneration of sensory axons. Among the release signs, only the reappearance of the grasp reflex is a reliable sign for indicating pathology of the nervous system. Senile tremor, a decline in the maintenance of thermal homoeostasis, an increasing frequency of orthostatic hypotension, and disorders of sleep are also commonly associated with aging.

Aged↗
PubMedDate not supplied

[Guillain-Barré syndrome as differential diagnosis of intervertebral disk-induced nerve root compression].

INTRODUCTION: Diagnosis of Guillian-Barré Syndrome usually is not difficult, but diagnostic failure occurs for the variable initial presentation. Diagnosis is based on physical examination showing loss of motor strength in more than one limb and loss of deep tendon reflexes. Ventilatory assistance, pharmacologic maintenance of cardiovascular homeostasis, corticosteroids, IgG and plasma exchange are the dominant therapeutic measures. CASE: This article reports on a case of a 59-year old surgeon suffering from degenerative disc disease in the lumbar spine. The patient developed a severe course of the Guillian-Barré Syndrome with persisting motor weakness of the legs. CONCLUSION: If the primary problem at presentation is limb and back pain the pathology appears to be in the musculoskeletal rather than in neurological system. The awareness of this presentation of Guillian-Barré-Syndrome will eliminate delay in diagnosis.

Diagnosis, Differential↗
PubMed1999

Friedreich's ataxia: clinical aspects and pathogenesis.

Friedreich's ataxia is the most frequent inherited ataxia in Caucasians. It is caused by deficiency of frataxin, a highly conserved nuclear-encoded protein localized in mitochondria. The DNA abnormality found in 98% of Friedreich's ataxia chromosomes is the unstable hyperexpansion of a GAA triplet repeat in the first intron of the frataxin gene. Most patients are homozygous for this repeat expansion. The expanded GAA repeat causes frataxin deficiency because it interferes with the transcription of the gene by adopting a non-B (probably triple helical) structure. Longer repeats cause a more profound frataxin deficiency and are associated with earlier onset and increased severity of the disease. Molecular testing has shown that the phenotypic spectrum of Friedreich's ataxia is wider than previously thought. Up to 10% of patients with recessive or sporadic degenerative ataxia who do not fulfill the Friedreich's ataxia diagnostic criteria are homozygous for expanded alleles at the Friedreich's ataxia locus. Late age of onset, retained tendon reflexes, and lack of pyramidal signs are among the atypical features observed in some patients with a positive molecular test. Yeast cells deficient in the frataxin homologue accumulate iron in mitochondria and show increased sensitivity to oxidative stress. This suggests that Friedreich's ataxia is caused by mitochondrial dysfunction and free radical toxicity, with consequent mitochondrial damage, axonal degeneration, and cell death.

Adaptor Proteins, Signal Transducing↗
PubMed1990

Conservative versus neurosurgical treatment of tethered cord patients.

We compared the outcome of neurosurgical release of a tethered spinal cord in 20 children with the neurological evolution of 21 other children known iwth a tethered spinal cord on nuclear magnetic resonance scan (NMR). Neurosurgery yielded stabilisation of the symptoms without any lasting improvement. Pre-operative conservative medical treatment had to be continued in all operated children. Three of the 20 operated children are showing signs of retethering despite appropriate neurosurgery, indicating that retethering should be considered as a major and frequent complication. In the majority of our children, symptomatic (re)tethering was recognised by the appearance of increased tendon reflexes and a progressive pes cavus, suggestive of an upper motor neuron disease involvement.

Child↗
PubMed1985

A case of childhood multiple sclerosis with peripheral neuropathy.

A twelve-year-old girl with multiple sclerosis and peripheral neuropathy is reported. When nine years old, she was diagnosed as having Devic disease (optic atrophy and transverse myelitis). During the three years after onset of her illness, she suffered from three relapses and remissions of her multiple sclerosis. On the third occasion, neurological examination revealed signs of cerebellar dysfunction including ataxic gait, nystagmus and dysmetria, and absence of all tendon reflexes with muscle weakness especially on the left side. Markedly slowed conduction velocity in her ulnar nerve especially on the left and elevated CSF protein were noted. Biopsied sural nerve showed decreased density of myelinated fibers and a selective loss of large diameter fibers. Electron microscopy disclosed onion-bulb formation, myelin debris within Schwann cell cytoplasm and demyelinated axons. These findings showed demyelination and remyelination of the peripheral nervous system in this patient with multiple sclerosis. We discuss the relation of multiple sclerosis and peripheral neuropathy.

Biopsy↗