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The clinical, pathological and genetic aspects of sporadic late onset cerebellar ataxia: observations on a series of ten patients.

Ten patients with sporadic late onset cerebellar ataxia (LOCA) are described. The mean age of onset was 50.4 +/- 7.13 years. The important clinical features were gait ataxia, poor coordination of hands, intention tremors, exaggerated deep tendon reflexes, extrapyramidal symptoms and extensor plantar responses. Computerised tomography (CT) scanning in one patient showed a low density mid-line lesion, suggesting early cerebellar atrophy. Histopathological examination in one patient, clinically diagnosed as multiple sclerosis, revealed complete loss of Purkinje cells from the cerebellar folia with gliosis in the molecular layer and loss of small granular neurones. A marked loss of the neurones from the olivary nuclei with astrocytic proliferation was also seen. The disorder is probably genetically determined although a single Mendelian inheritance is unlikely in the absence of recurrence in the first degree relatives. Recurrence risks for gentic counselling are suggested.

Adult↗

Outcome and neurological sequelae of patients after tetanus.

From 1969-1985, 106 people contracted tetanus in Finland. The outcome of the disease was good in 78 cases (returned to work), poor in 27 (12 died, 5 institutionalized and 10 retired) and unknown in 1. Poor outcome was the result of a disease requiring respirator treatment. Other clinical factors significantly correlated with poor outcome were blood pressure lability, hyperglycemia, hyperthermia, tachycardia and anticoagulation therapy. Forty people who were representative of the whole series with regard to sex, age and severity of disease attended a follow-up study on average 7 years and 4 months later. Forty age- and sex-matched controls had the same examinations, and compared with them, the 40 patients still had significantly more muscle fatigue and cramps, nervousness, decreased mental capacity and difficulties in balance, speech and memory. They also had more clinical findings, such as peripheral paresis, muscular atrophy, decreased or absent tendon reflexes and decreased mental capacity than the controls.

Adolescent↗

Adult Chédiak-Higashi syndrome presenting as parkinsonism and dementia.

Chédiak-Higashi syndrome (CHS) in children can be a fatal disease. We describe the oldest known CHS patient first seen with a neurologic disorder in early adult life. From the age of 22, this 39-year-old woman developed mental deterioration, parkinsonism including resting tremor at the tongue, mandible, and hands, oculogyric crisis, muscular atrophy of limbs, and loss of tendon reflexes. MRI showed marked temporal dominant brain atrophy and diffuse spinal cord atrophy. Partial albinism, pan-leukocytic giant granules, and profoundly decreased NK-cell activity were compatible with childhood CHS, but apparently normal neutrophil function prolonged her survival. Stimulated proliferation of lymphocytes was less than 40% that of normal controls.

Adult↗

Hereditary ataxias and paraplegias in Valle d'Aosta, Italy: a study of prevalence and disability.

INTRODUCTION: a study was conducted in the Valle d'Aosta Region, Italy, (115270 inhabitants) to determine the prevalence of hereditary ataxias (HA) and hereditary spastic paraplegias (HSP), and the degree of disability they cause. METHODS: we identified all patients with suspected HA or HSP referred from 1981 to 1991 to in- and out-patient departments, EEG, EMG, and CT-scan services, and centres for the handicapped. Harding's criteria were followed for diagnosis and classification. RESULTS: at the prevalence day, 17 patients were alive, with a prevalence ratio of 14.8/100,000 population. There were 2 cases of Friedreich's ataxia (FA), 1 of early onset cerebellar ataxia with retained tendon reflexes (EOCA), 1 of autosomal dominant cerebellar ataxia (ADCA), 8 of sporadic idiopathic late onset cerebellar ataxias, and 5 of HSP. CONCLUSIONS: epidemiological studies on HA and HSP show highly variable prevalence ratios, which could be due in part to the inclusion of sporadic cases. FA, EOCA and ADCA have similar prevalence ratios in most studies.

Adolescent↗

Clinical features and natural history of spinocerebellar ataxia type 1.

SCA1 is a dominant spinocerebellar ataxia (SCA) and a multi-systemic syndrome caused by abnormal expansion of unstable CAG repeat in a novel gene located on chromosome 6p22-p23. We clinically studied 35 Japanese SCA1 patients who were assumed to have come from a common origin. The age at onset ranged from 15-63 years, and significantly correlated with CAG repeat units of mutant alleles. Ataxia was the initial symptom, and the majority of patients had a similar history of signs and symptoms. Nystagmus was at first minimal, later attenuated, and a slow saccade followed. Limb tendon reflexes were mostly hyperactive and depressed with the development of diffuse amyotrophy. The cardinal feature was ataxia-hyperreflexia-late slow saccade syndrome with terminal amyotrophy. Although the phenotype of SCA1 overlaps with those of other dominant SCAs, some facets of the neurological events differ from either SCA2 with ataxia-hyporeflexia-slow saccade syndrome, or early-onset Machado-Joseph disease with dystonia-bradykinesia-spasticity syndrome.

Adolescent↗

Increased risk of sensory neuropathy in workers with chloracne after exposure to 2,3,7,8-polychlorinated dioxins and furans.

OBJECTIVE: The existence of a peripheral neuropathy after exposure to polychlorinated dioxins (PCDD) is still discussed, as studies concerning dioxin effects on the peripheral nervous system are rare and contradictory. MATERIAL AND METHODS: Clinical and neurophysiological examinations (motor conduction velocity of the peroneal nerve, sensory conduction velocities of the sural and ulnar nerves) were made in 156 dioxin exposed workers (42 with, 114 without cloracne) from one pesticide producing plant. Because of known risk factors for peripheral neuropathy, 7 workers with and 28 without cloracne were excluded from further analysis. RESULTS: Workers with chloracne had a significantly higher exposure against PCDD as documented by back calculated lipid levels. They complained significantly more often of sexual impotence (28.6% compared to 5.8% of workers without chloracne, P<0.001), had significantly more frequent clinical signs of a sensory neuropathy (= abnormal sensory findings plus deep tendon reflex abnormalities) restricted to the legs (17.1% compared to 1.2%, P<0.001), had significantly more frequent > or =2 neurophysiologic abnormalities (34.3% compared to 14.0%, P<0.025), and had significantly lower mean amplitudes of the motor compound muscle potential of the peroneal nerve. CONCLUSION: PCDD has a mild toxic effect on the peripheral nervous system manifesting as mild sensory neuropathy of the legs in a minority of the most severely exposed persons.

Acne Vulgaris↗

Laminin alpha2 deficiency-associated muscular dystrophy in a Maine coon cat.

A European case of laminin alpha2 deficiency-associated muscular dystrophy in a 12-month-old, female Maine coon pedigree cat is reported. The history and eventual clinical presentation of this cat differed from those of two cats reported in the USA. In this case, the myopathy was characterised by progressively worsening weakness, muscle atrophy and joint contracture. Tendon reflexes were diminished, and motor nerve conduction velocities were slowed. Muscle biopsy demonstrated a dystrophic phenotype with endomysial fibrosis. Occasional thinly myelinated nerve fibres were present within a peripheral nerve specimen. Poorly myelinated fibres were also found at the root level on necropsy specimens. Immunohistochemical staining revealed the absence of laminin alpha2. The cat's family history did not indicate genetic transmission of the disease.

Animals↗

Friedreich's ataxia. A clinical review with neurophysiological and echocardiographic findings.

In a review of twelve cases of Friedreich's ataxia, the important criteria for early diagnosis were identified. Clinical signs included absent tendon reflexes, ataxic gait, and a positive Romberg test. Nerve conduction velocities showed absent or severely slowed sensory conduction, with normal motor conduction. In addition, echocardiographic changes of symmetrical hypertrophic cardiomyopathy were found.

Action Potentials↗

Arch fingerprints, hypotonia, and areflexia associated with X linked mental retardation.

A syndrome with distinctive facies, poor muscle tone, absent deep tendon reflexes, tapered fingers, excessive fingerprint arches, genu valgum and mild-moderate mental retardation has occurred in four males in two generations of a white family of European ancestry. The facies are characterised by square configuration, tented upper lip, and thickening of the helices, upper eyelids, and alae nasi. At birth and at maturity, growth (head circumference, height, weight) of affected males is comparable to or greater than unaffected male sibs. Moderate impairment of cognitive function was documented (IQ scores between 40-51). Carriers show no heterozygote manifestations. This X linked condition appears to be different from other syndromes with mental retardation, although there are certain similarities with the alpha thalassaemia-mental retardation syndrome (ATR-X). Linkage analysis found tight linkage to DXS1166 and DXS995 in Xq13 and Xq21 respectively.

Abnormalities, Multiple↗

Neurophysiological testing correlates with clinical examination according to fibre type involvement and severity in sensory neuropathy.

OBJECTIVE: To investigate a comprehensive battery of neurophysiological tests for objective evaluation of sensory neuropathies including fibre type involvement and severity, and to determine the relation between neurophysiological data and clinical examination. METHODS: 45 patients referred for sensory neuropathy were studied using a standardised clinical evaluation of large and small fibre symptoms and an original neurophysiological battery. Clinical evaluation included: assessment of tactile, vibratory, and pin sensation; tendon reflexes; toe position sense; ataxia score; pain level; and presence of trophic, vasomotor, or sudomotor abnormalities. The neurophysiological battery included: recording of large fibre and small fibre components of the sural sensory nerve action potential; somatosensory evoked cortical potentials and soleus H reflex following tibial nerve electrical stimulation; laser evoked potentials following Nd:YAG laser stimulation of the foot; and plantar sympathetic skin response to median nerve stimulation. Neuropathy was classified according to the predominantly affected fibre type, and a severity score was established based on clinical and neurophysiological abnormalities. RESULTS: On clinical examination there were 22 patients with large fibre sensory neuropathy (LFSN), 18 with mixed sensory neuropathy (MSN), and five with small fibre sensory neuropathy (SFSN). Neurophysiological classification identified 25 patients with LFSN, 13 with MSN, and seven with SFSN. Clinical and neurophysiological classifications and severity scores were correlated, whatever the type of neuropathy. CONCLUSIONS: The correlation between clinical examination and the results of an original neurophysiological test battery offers a comprehensive clinical and neurophysiological approach to the objective assessment of peripheral neuropathies according to fibre type involvement and overall severity.

Adult↗

Generalised anhidrosis: different lesion sites demonstrated by microneurography and skin biopsy.

Generalised anhidrosis (GA) shows a uniform clinical picture whether the pathogenesis involves intrinsic abnormalities of sweat glands or postganglionic sympathetic cholinergic nerve dysfunction. We describe two patients who presented intolerance to heat and anhidrosis. In the first patient, symptoms started at 33 years of age, and were associated with absent tendon reflexes and a mydriatic right pupil unreactive to light. The other patient had been unable to sweat since birth. GA was diagnosed on the basis of clinical findings and thermoregulatory tests. Microneurography and morphological analysis of the skin and its innervation disclosed a different lesion site underlying GA in the two patients, and distinguished between a postganglionic autonomic nerve fibre lesion and sweat gland dysfunction.

Adult↗

A study of a respiratory related variation of muscle tone during the decrement of decerebrate tonicity in ECT.

An oscillating decerebrate tonicity following the clonus phase in electroplexy was found to occur in the upper limbs, their tendon reflexes and the jaw; this increased with each expiration and decreased with inspiration. The times of these occurrences in the upper limbs were measured in groups where no anaesthesia, diazepam or methohexital were used. The mean times of their onset and end were related to other phenomena of ECT. The times of occurrence and duration of decerebrate tonicity were established and compared in the three cohorts. There was a definite relationship to the onset of respiratory rhythmicity in all three groups. The evidence for the existence of decerebrate tonicity and atonicity are discussed from experimental contributions and more recent clinical evidence of the clonus phase as an example of an oscillation between tonic and atonic decerebrate states. Further clinical and experimental data are discussed which show connections between the decerebrate state, cerebral and cerebellar functions, respiratory centres, brain-stem and gravity afferents during rest and locomotion. An explanation is offered that the oscillatory phenomena are probably a mechanism to aid respiration and motor efficiency.

Brain Stem↗

Flaccid paraplegia: a feature of spinal cord lesions in Holmes-Adie syndrome and tabes dorsalis.

In a patient with Holmes-Adie syndrome, and in another with tabes dorsalis, a transverse cord lesion resulted in a severe, but flaccid paraplegia with absent tendon reflexes. Flexor spasms were severe in both patients, but spasticity was absent. The significance of these observations is discussed in relation to the functional and anatomical disorder in these two syndromes.

Adie Syndrome↗

Neurological asymmetries immediately after unilateral ECT.

Twenty-nine right handed patients were examined neurologically before and immediately after each of 62 unilateral ECTs to the dominant and non-dominant hemispheres. Most convulsions were followed by signs of transitory neurological dysfunction referable to the treated hemisphere. These signs included deep tendon reflex asymmetry, hemiparesis, tactile and visual inattention, and homonymous hemianopia. After treatment to the right hemisphere some patients had left visuospatial neglect, while all patients who had dominant hemisphere ECT were transiently dysphasic. All neurological abnormalities tested resolved within 20 minutes of treatment.

Aphasia↗

Peroneal muscular atrophy with pyramidal features.

Twenty-five cases of peroneal muscular atrophy with pyramidal features from 15 families are described. This disorder has been referred to as hereditary motor and sensory neuropathy (HMSN) type V by Dyck. Onset was usually in the first two decades of life with difficulty in walking. The clinical syndrome superficially resembled that of HMSN types I and II with distal wasting and weakness involving the legs more than the arms. The tendon reflexes in the upper limbs and at the knee tended to be normal or increased but the ankle jerks were often absent. The plantar responses were extensor in 22 patients, absent in two and flexor in one. Increased tone and weakness in the proximal lower limb muscles were found in about 30% of cases. Mean motor nerve conduction velocity was lower than in normal controls and sensory nerve action potentials were reduced in amplitude or absent in two thirds of the patients studied. Inheritance was autosomal dominant in the majority of families. The disorder was slowly progressive but did not lead to severe disability.

Adolescent↗

Delayed neuropathy after organophosphorus insecticide (Dipterex) poisoning: a clinical, electrophysiological and nerve biopsy study.

Clinical, electrophysiological and histological findings in four patients accidentally poisoned with the organophosphorus insecticide Dipterex are reported. Three to five weeks after insecticide ingestion signs of a distal sensorimotor (preponderantly motor) neuropathy occurred. The patients complained of paraesthesia in the lower limbs, and two of them of very disagreeable pricking sensation in the soles of the feet, responsive to carbamazepine. They showed distal weakness mainly of the legs, footdrop , difficult gait and muscle hypotonia. Ankle jerk was abolished while other tendon reflexes persisted. Two months or even later after poisoning, knee jerks in all the patients were very brisk and more and less accompanied by other pyramidal signs (patellar clonus, abolishment of abdominal cutaneous reflexes, Babinski's sign). Clinical, electrophysiological and nerve biopsy data revealed a "dying-back" neuropathy in our patients. Distal muscle fatigue was confirmed by failure of neuromuscular transmission on repetitive nerve stimulation.

Adult↗

An hereditary sensory and autonomic neuropathy transmitted as an X-linked recessive trait.

Five members of a single family presented with neuropathic deformities and ulceration of the feet developing in the first and second decades of life, and progressed slowly over many years. In this form of hereditary sensory and autonomic neuropathy, there was minimal tendon reflex impairment, cutaneous sensory impairment was restricted to the feet, and there was no autonomic dysfunction. The only neurophysiological abnormality was that of reduced or absent sural nerve sensory action potentials. Sural nerve biopsies taken from two affected family members showed changes of a chronic neuropathy with loss of myelinated fibres, particularly affecting those of small diameter. Unmyelinated fibres were present in normal numbers. This condition differed from other forms of hereditary sensory and autonomic neuropathy having an X-linked recessive mode of inheritance.

Adolescent↗

Central motor conduction in degenerative ataxic disorders: a magnetic stimulation study.

Central motor conduction to small hand muscles was measured using magnetic stimulation of the motor cortex and electrical stimulation of proximal motor roots in 11 patients with Friedreich's ataxia, 10 patients with early onset cerebellar ataxia with retained tendon reflexes (EOCA) and 13 patients with late onset degenerative cerebellar disease (LOCD). Central motor conduction was abnormal in 91% with Friedreich's ataxia, 70% with EOCA and 38% with LOCD. Central motor conduction abnormalities were not specific to individual disorders but were more severe and were related to disease duration in Friedreich's ataxia and EOCA.

Adult↗