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PubMed1981

The differential diagnosis of congenital analgesia and other diseases with diminished pain perception in childhood. Case report and review.

This paper reports the case of a boy aged 10 months who suffers from congenital analgesia in its pure form. All clinical, biochemical, neuro=physiological and histological data considered to be significant in the differential diagnosis are presented. The findings in all diseases in which impairment of pain sensation occurs are tabulated. 38 patients meet the diagnostic criteria for pure congenital analgesia. The diagnostic criteria are generalized indifference to pain dating from birth; no impairment of other sensory modalities; normal intelligence; normal deep tendon reflexes; no visceral pain perception; normal skin biopsy; no diminution of myelinated or un-myelinated nerve fibres in sural nerve biopsy; normal motor and sensory nerve conduction velocities and normal karyotype. The mode of inheritance remains unclear, but it is assumed, that congenital analgesia might be an autosomal-recessively inherited disease.

Child↗
PubMed1981

Sensory ganglioneuropathy in infantile spinal muscular atrophy. Light and electronmicroscopic findings in two cases.

Light and electronmicroscopic findings in two cases. Neuropediatrics 12: 215-31 (1981). Two cases of infantile spinal muscular atrophy (Werdnig-Hoffmann disease) are described in unrelated children deceased at 11 months (acute clinical onset at 6 months) and 2 years (onset at birth). Severe respiratory difficulties, hypotonia, muscular weakness and depressed tendon reflexes were the main clinical features. Bulbar palsy, bilateral ptosis, pale optic discs and atactic movements of the hands were observed in the child deceased at 11 months. Besides severe loss of anterior horn cells and neurogenic muscle atrophy there was evidence of an extensive sensory involvement in both cases. Shrinkage, vacuolation as well as chromatolytic changes of dorsal root ganglion cells, together with the evidence of a primary axonal damage in sural nerve biopsies were interpreted in terms of ganglioneuropathy of the primary sensory neurons. An invasion of fibrous astrocytes into dorsal roots constituted another striking anomaly in one case as well as a pronounced degeneration of cranial nerves V and VIII in the other case, a finding not hitherto reported in Werdnig-Hoffmann disease.

Brain↗
PubMed1990

Spinal muscular atrophy in African children.

Forty-five African children with SMA were seen over a period of five years. Fifteen had severe infantile form (Group 1), 19 intermediate (Group 2), 9 juvenile (Group 3) and 2 cervical type. A positive family history was obtained in only 9% of patients. The female/male ratio was 1:1.7. The age of onset was under four months in Group 1, between 5-24 months in Group 2. In 77% of Group 3 onset was between 5-24 months, 22% between 25-48 months. The lower limbs were more severely affected than upper limbs in all except the two patients with cervical SMA, proximal muscles more than distal in 82% and proximal and distal muscle were equally affected in 18%. Bulbar weakness was present in 73% and facial weakness in 80% of Group 1 patients only. Fasciculation of tongue occurred in 50% of Group 1, 42% of Group 2 and 44% of Group 3 patients. Tremor of hands was seen in none of the patients in Group 1, 58% in Group 2 and 66% in Group 3. Tendon reflexes were absent or depressed in all except one patient in Group 2 and were normal in the legs of the two patients with cervical SMA. The blood CK was elevated in 26% of patients. An ECG "tremor" was present in 26% of patients in Group 1, 68% in Group 2 and 66% in Group 3. Four patients (all in Group 1) died of pneumonia; the outcome in the others is not known.(ABSTRACT TRUNCATED AT 250 WORDS)

Africa↗
PubMed1980

Increased incidence of retinopathy in diabetics with elevated blood pressure. A six-year follow-up study in Pima Indians.

The incidence of retinopathy was assessed in 188 diabetic and 284 nondiabetic Pima Indian adults six years after an initial examination had shown each to be free of retinopathy. Exminations included direct ophthalmoscopy through dilated pupils. The incidence of retinal lesions was strongly related to the presence of diabetes and, among the diabetic subjects, to insulin treatment, disease duration, plasma glucose concentration, and presence of other complications such as proteinuria, loss of deep tendon reflexes, and increased vibration-sensation threshold. In diabetic subjects not taking insulin, the incidence of exudates in those with systolic blood pressures of at least 145 mm Hg was more than twice that of those with pressures of less than 125 mm Hg. This association persisted when assessed within categories of subjects stratified according to 13 potentially confounding variables, suggesting that control of blood pressure may reduce the incidence of retinal exudates in diabetics not treated with insulin.

Adult↗
PubMed1996

Clinical and genetic abnormalities in patients with Friedreich's ataxia.

BACKGROUND: Friedreich's ataxia, the most common inherited ataxia, is associated with a mutation that consists of an unstable expansion of GAA repeats in the first intron of the frataxin gene on chromosome 9, which encodes a protein of unknown function. METHODS: We studied 187 patients with autosomal recessive ataxia, determined the size of the GAA expansions, and analyzed the clinical manifestations in relation to the number of GAA repeats and the duration of disease. RESULTS: One hundred forty of the 187 patients, with ages at onset ranging from 2 to 51 years, were homozygous for a GAA expansion that had 120 to 1700 repeats of the trinucleotides. About one quarter of the patients, despite being homozygous, had atypical Friedreich's ataxia; they were older at presentation and had intact tendon reflexes. Larger GAA expansions correlated with earlier age at onset and shorter times to loss of ambulation. The size of the GAA expansions (and particularly that of the smaller of each pair) was associated with the frequency of cardiomyopathy and loss of reflexes in the upper limbs. The GAA repeats were unstable during transmission. CONCLUSIONS: The clinical spectrum of Friedreich's ataxia is broader than previously recognized, and the direct molecular test for the GAA expansion on chromosome 9 is useful for diagnosis, determination of prognosis, and genetic counseling.

Adolescent↗
PubMed2006

Recessive symptomatic focal epilepsy and mutant contactin-associated protein-like 2.

Contactin-associated protein-like 2 (CASPR2) is encoded by CNTNAP2 and clusters voltage-gated potassium channels (K(v)1.1) at the nodes of Ranvier. We report a homozygous mutation of CNTNAP2 in Old Order Amish children with cortical dysplasia, focal epilepsy, relative macrocephaly, and diminished deep-tendon reflexes. Intractable focal seizures began in early childhood, after which language regression, hyperactivity, impulsive and aggressive behavior, and mental retardation developed in all children. Resective surgery did not prevent the recurrence of seizures. Temporal-lobe specimens showed evidence of abnormalities of neuronal migration and structure, widespread astrogliosis, and reduced expression of CASPR2.

Child↗
PubMed1999

Deficit of in vivo mitochondrial ATP production in patients with Friedreich ataxia.

Friedreich ataxia (FRDA), the most common of the inherited ataxias, is an autosomal recessive degenerative disorder, characterized clinically by onset before the age of 25 of progressive gait and limb ataxia, absence of deep tendon reflexes, extensor plantar responses, and loss of position and vibration sense in the lower limbs. FRDA is caused by a GAA triplet expansion in the first intron of the FRDA gene on chromosome 9q13 in 97% of patients. The FRDA gene encodes a widely expressed 210-aa protein, frataxin, which is located in mitochondria and is severely reduced in FRDA patients. Frataxin function is still unknown but the knockout of the yeast frataxin homologue gene (YFH1) showed a severe defect of mitochondrial respiration and loss of mtDNA associated with elevated intramitochondrial iron. Here we report in vivo evidence of impaired mitochondrial respiration in skeletal muscle of FRDA patients. Using phosphorus magnetic resonance spectroscopy we demonstrated a maximum rate of muscle mitochondrial ATP production (V(max)) below the normal range in all 12 FRDA patients and a strong negative correlation between mitochondrial V(max) and the number of GAA repeats in the smaller allele. Our results show that FRDA is a nuclear-encoded mitochondrial disorder affecting oxidative phosphorylation and give a rationale for treatments aimed to improve mitochondrial function in this condition.

Adaptor Proteins, Signal Transducing↗
PubMed2002

Multiple sclerosis-like disease secondary to alpha interferon.

PURPOSE: To describe bilateral optic neuritis that occurred as an adverse effect of recombinant and natural interferon alpha administration. METHODS: Report of two cases. Case 1, a 62-year-old woman, developed bilateral optic neuritis with decreased sensation of vibration and increased deep tendon reflex in the lower extremities after a seven-month use of recombinant interferon alpha-2a for chronic active hepatitis C. Case 2, a 29-year-old woman, developed bilateral optic neuritis combined with numbness of the lower extremities as well as bowel and bladder dysfunction after a 22-month use of recombinant interferon alpha-2b for chronic myelogenous leukemia. After a two-month interruption of interferon administration, natural interferon alpha was given but followed by another episode of the same neurological manifestations. RESULTS: In both cases, magnetic resonance imaging demonstrated multiple small high-intensity areas in the cerebral white matter and spinal cord, while cerebrospinal fluid examination disclosed mononuclear cell increase and protein elevation including myelin basic protein, all of which simulated the features of multiple sclerosis. The two patients underwent several courses of pulse corticosteroid therapy, each course consisting of three days of methylprednisolone 1000 mg daily, resulting in visual recovery to some extent. CONCLUSIONS: Optic neuritis in combination with other neurological signs, simulating multiple sclerosis, should be included in the list of adverse effects of recombinant and natural interferon alpha administration.

Adult↗
PubMedDate not supplied

Neurobehavioral estimation of children with life-long increased lead exposure.

A battery of neurobehavioral examinations was carried out on 30 children who were 6-11 yr of age and who had resided near a lead smelter all their lives. Their blood lead levels were 35-60 micrograms/100 ml and erythrocyte protoporphyrin levels were greater than 100 micrograms/100 ml. Neurological examination revealed that they had a significantly higher incidence of pathological findings (e.g., muscle hypotonia, increased tendon reflexes, dysarthria, and dysdiadochokinesia) than children from an unpolluted area who were matched for age, sex, family size, and educational and socioeconomic status of the parents, but who had normal erythrocyte protoporphyrin levels. The children with elevated blood lead levels showed, after assessment by the Oseretsky test, retardation of motor maturation; they also scored higher on the minimal brain damage scale of the Rutter behavioral questionnaire. These differences persisted at a 4-yr follow-up, and their school performance was consistently poorer than that of the controls.

Child↗
PubMed2005

Closure of a patent foramen ovale: effective therapy of migraine and occipital stroke.

Whether stroke in a patient with migraine and patent foramen ovale (PFO) is due to PFO or migraine is difficult to decide. In a 33-year-old woman with migraine with aura, a visual field defect developed acutely. Neurological investigation revealed double vision when looking to the left and exaggerated patella tendon reflexes. Since then the patient complained about permanent visual impairment. CT- and MRI-scans of the brain showed a right occipital ischemic stroke. Intensive search for risk factors revealed cigarette smoking and chronic hypovolemia On transesophageal echocardiography an inter-atrial hypermobile septum and a PFO were detected. The patient underwent closure of the PFO by means of an Amplatzer PFO occluder nine weeks after the stroke. Since then she did not experience a further cerebrovascular event or migraine attack. This case shows that in a patient with PFO and migraine with aura, stroke may be attributable to migraine rather than to PFO. Occlusion of the PFO may reduce the frequency and intensity of migraine attacks.

Adult↗
PubMed1998

Assessment of peripheral nerve function in an Ecuadorian rural population exposed to pesticides.

To explore the peripheral nervous system effects of regular agricultural pesticide use, a cross-sectional survey was conducted in highland Ecuador. Participants were 144 occupationally exposed farm members, 30 female farm members with little direct exposure, and 72 unexposed local town residents, frequency matched to the exposed people on age, sex, and education. Organophosphorus and carbamate insecticides and dithiocarbamate fungicides accounted for the majority of pesticide applications, with leaking backpack sprayers, minimal use of personal protective equipment, and frequent dermal contact being the norm. In polytomous logistic regression analyses, applicators had significantly greater odds for more current peripheral nerve symptoms (odds ratio OR = 3.1), signs of poor coordination (OR = 4.3), abnormal deep tendon reflexes (OR = 2.9), and reduced power (OR = 2.1) compared to controls. Mean toe vibration threshold scores, on a logarithmic scale, were significantly higher among applicators (beta = 0.035) and those reporting previous pesticide poisonings (beta = 0.074). Such indicators of peripheral nervous system effects may be due to a variety of factors, including high pesticide exposure conditions.

Adult↗
PubMed1999

Neurological features of cerebral malaria in Nigerian children.

Cerebral malaria is one of the commonest causes of an acute neurological syndrome in malaria-endemic areas. However, there are few detailed reports of findings on clinical neurological examination of the condition. The neurological features of cerebral malaria in 103 children aged 5 years or less were studied in Ibadan, Nigeria, an area of high malaria transmission. The correlation of these features with prognosis was also studied. Convulsions occurred in 87% of subjects and were in most cases of a generalized tonic-clinic nature. Abnormalities of posture were observed in 41%, abnormal tone in 70% and abnormal deep tendon reflexes in 74%. Absent corneal reflexes were found in about 14%. The time interval between the last seizure episode and presentation in hospital, abnormal posture (decerebrate or decorticate), absence of corneal reflex and depth and duration of coma were indicators of poor prognosis. In this study, cerebral malaria presented with non-specific features of diffuse, symmetrical, upper motor neurone dysfunction, and some specific neurological features were associated with poor prognosis. It is important that cerebral malaria be considered in any child with features of acute encephalopathy in a malaria-endemic area. Careful clinical examination of such children is essential as neurological features of the condition may provide a clue to prognosis.

Child, Preschool↗
PubMedDate not supplied

Peripheral neuropathy during alpha-interferon therapy in a child with Hodgkin's disease.

Peripheral neuropathy is one of the rarely reported neurological complications of interferon therapy. The authors report such a case in a 15-year-old boy during alpha-interferon therapy for Hodgkin's disease. He received alpha-interferon at a dose of 1.8 million units/day 5 times a week by subcutaneous injections as adjuvant immunotherapy post autologous stem cell transplant. Twenty months after the initiation of therapy, he complained of severe pain in his lower distal extremities. Neurological examination revealed the absence of deep tendon reflexes. A nerve conduction study showed a sensorial, polyneuropathic involvement in the lower extremities. Within 4 weeks after the stopping of interferon, his pain improved, and recovery was also seen by nerve conduction studies. Symptoms reappeared at the resumption of interferon treatment. This study suggests that peripheral neuropathy may rarely occur in patients given long-term interferon treatment at high cumulative dosage.

Adolescent↗
PubMed2005

Clinicopathological and virological analyses of familial human T-lymphotropic virus type I--associated polyneuropathy.

Human T-lymphotropic virus type I (HTLV-I) is known to be the causative agent of the chronic myelopathy, HTLV-I--associated myelopathy (HAM), and on rare occasions infection is also associated with the development of polyneuropathy. Here the authors present an HTLV-I--positive family of whom four members developed a chronic demyelinating polyneuropathy without HAM. Four female patients in a family from Hokkaido in Japan developed distal dominant paresthesia and muscle weakness in the second and third decades of their life. Neurological findings at ages ranging from 50 to 65 years included mild painful sensorimotor disturbances with atrophy of the distal parts of the extremities but without pyramidal signs or hyperactive tendon reflexes. Magnetic resonance imaging (MRI) findings of brain and spinal cord were unremarkable. Serum HTLV-I antibody levels were elevated at 1:8192 to 1:32,768, whereas those in cerebrospinal fluid were low at 1:4 to 1:8. Electrophysiological studies revealed polyphasic compound muscle action potentials with denervation potentials on nerve conduction studies and neurogenic patterns by electromyography, which were consistent with signs of chronic motor dominant demyelinating polyneuropathy. Sural nerve biopsy showed decreased myelinated fibers, occurrence of globule formation, myelin ovoid and remyelinated fibers, and an infiltration of CD68-positive macrophages with occasional CD4-positive T cells in the nerve fascicles. The polyneuropathy was responsive to steroid therapy. Analyses of serological human leukocyte antigen (HLA) types indicated that none of the patients possessed a high-risk HLA type known to be associated with adult T-cell leukemia (ATL), whereas they did have high responsive alleles to HTLV-I env similar to that observed in HAM. Nucleotide sequence analysis of the HTLV-I tax region demonstrated the B subgroup in all patients. This study suggests that HTLV-I infection can result in the development of a familial form of polyneuropathy that is associated with distinct HLA class I alleles, which might possibly involve a distinct virus subtype.

Antibodies, Viral↗
PubMed2006

Clinical symptoms and the odds of human T-cell lymphotropic virus type 1-associated myelopathy/ tropical spastic paraparesis (HAM/TSP) in healthy virus carriers: application of best-fit logistic regression equation based on host genotype, age, and provirus load.

The authors have previously developed a logistic regression equation to predict the odds that a human T-cell lymphotropic virus type 1 (HTLV-1)-infected individual of specified genotype, age, and provirus load has HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) in southern Japan. This study evaluated whether this equation is useful predictor for monitoring asymptomatic HTLV-1-seropositive carriers (HCs) in the same population. The authors genotyped 181 HCs for each HAM/TSP-associated gene (tumor necrosis factor [TNF]-alpha-863A/C, stromal cell-derived factor 1 (SDF-1) +801G/A, human leukocyte antigen [HLA]-A*02, HLA-Cw*08, HTLV-1 tax subgroup) and measured HTLV-1 provirus load in peripheral blood mononuclear cells using real-time polymerase chain reaction (PCR). Finally, the odds of HAM/TSP for each subject were calculated by using the equation and compared the results with clinical symptoms and laboratory findings. Although no clear difference was seen between the odds of HAM/TSP and either sex, family history of HAM/TSP or adult T-cell lenkemia (ATL), history of blood transfusion, it was found that brisk patellar deep tendon reflexes, which suggest latent central nervous system compromise, and flower cell-like abnormal lymphocytes, which is the morphological characteristic of ATL cells, were associated with a higher odds of HAM/TSP. The best-fit logistic regression equation may be useful for detecting subclinical abnormalities in HCs in southern Japan.

Adult↗
PubMed2001

Arterial hypertension as a risk factor for chronic symmetric polyneuropathy.

OBJECTIVE: To assess whether arterial hypertension (AH) is an independent risk factor for chronic symmetric polyneuropathy (CSP) in the elderly. BACKGROUND: A strong relationship has been detected between AH and distal symmetric polyneuropathy in insulin-dependent and non-insulin-dependent diabetes. However, the correlation between AH and polyneuropathy caused by other clinical conditions has not yet been studied. METHODS: Four thousand one hundred and ninety-one subjects aged > or = 55 years seen in office consultations by 25 general practitioners (GPs) from two separate areas in Italy were interviewed, using a pretested semistructured questionnaire covering conditions commonly associated with neuropathy and symptoms of peripheral nerve disease. A neurologist later visited individuals with > or = 2 symptoms of polyneuropathy and a diagnosis of CSP was made in the presence of bilateral, fairly symmetric impairment of at least two among strength, sensation and tendon reflexes. AH was ascertained when known to the GP and/or if the patient was being treated with antihypertensive drugs. RESULTS: One hundred and fifty one subjects had CSP (3.6%). Diabetes was the commonest associated condition (18%). AH was present in 47 patients with CSP (31%). The odds ratio (OR) of AH in patients with CSP was 4.5 [95% confidence interval (CI) 3.1-6.6]. The OR of AH was 3.2 (95% CI 1.5-6.9) in patients with diabetes, and 5.7 (95% CI 3.6-9.3) in those without diabetes. The OR of AH was 4.8 (95% CI 4.4-5.2) after adjusting for the commonest risk factors for CSP. CONCLUSION: AH may be an independent risk factor for CSP in the elderly.

Aged↗
PubMed2003

Shoulder pain in hemiplegia revisited: contribution of functional electrical stimulation and other therapies.

OBJECTIVES: Post-stroke shoulder pain is probably the most frequent complication in hemiplegia and has repercussions on motor rehabilitation and the psychological equilibrium of the patient. The strategies for prevention and treatment are presented. AETIOLOGY: Among the various factors contributing to the occurrence of shoulder pain in hemiplegia, some are related to the joint, such as lesion of the rotator cuff tendons, reflex sympathetic dystrophy, inferior-anterior subluxation of the head of the humerus, whereas others are related to the neurologic lesion such as central post-stroke pain, lack of sensibility, unilateral neglect and spasticity. PREVENTION: Efforts should be made from the start to keep the shoulder in an ideal position at all times and movement of the shoulder and upper limb should be carried out with care. TREATMENT: Will be aimed to the cause of pain and passive or active range of motion exercises will be encouraged. Physical, medical and surgical treatments have improved over the last few decades. Functional electrical stimulation in patients with shoulder pain and subluxation, applied early after onset of the stroke, has shown beneficial positive effects on subluxation, pain and mobility. Efforts should therefore be made to better understand the post-stroke shoulder pain in order to provide better outcomes of rehabilitation and thus improve quality of life for patients.

Electric Stimulation Therapy↗
PubMed2006

Correlation between impairment and motor performance during reaching tasks in subjects with spastic hemiparesis.

OBJECTIVE: The main purposes of this study were to examine, in subjects with chronic hemiparesis following a stroke: (i) the correlations between tests of muscle tone, stiffness, spasticity, paresis and co-contraction, and (ii) the correlations of these tests and measurements of impairment to upper extremity motor performance. DESIGN: Prospective, cross-sectional, correlation matrix using sample of convenience. SUBJECTS: Thirteen subjects with chronic hemiparesis secondary to a cerebrovascular accident (stroke) were tested. METHODS: Subjects were assessed using the Fugl-Meyer Upper Extremity Motor Assessment, modified Ashworth scale, deep tendon reflexes, and muscle characteristics that included quantification of muscle stiffness, paresis and co-contraction during a voluntary reaching task and during passive movements. Surface electromyographic and myotonometric muscle stiffness data were obtained during movement trials. RESULTS: Biceps and triceps brachii muscle paresis and excess biceps brachii co-contraction during voluntary reaching had the highest correlations to decreased motor performance. Muscle tone measurements did not have significant correlations to upper extremity performance. CONCLUSION: Paresis of elbow flexors and extensors and excess co-contraction of the biceps brachii during voluntary reaching appear to be most predictive of upper extremity motor performance. Results are discussed in relation to the specific challenges these findings pose for spastic paresis clinical management.

Aged↗