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At least 1,009 records · Page 56Linked to original sources
PubMed2006

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy: an imaging mimic of multiple sclerosis. A report of two cases.

OBJECTIVE AND IMPORTANCE: To describe the imaging findings of two cases of cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) mimicking multiple sclerosis. CLINICAL PRESENTATION AND INTERVENTION: Two cases presenting with neurological signs and symptoms were referred for magnetic resonance imaging (MRI) evaluation of the brain. Case 1 was a 36-year-old female patient presenting with recurrent headaches and recent onset numbness in the fingers of the right hand. Neurological examination showed a mild sensory deficit in the right hand. Case 2 was a 31-year-old female patient presenting with attacks of right-sided numbness of the face and body. The neurological examination revealed a sensory loss in the face and brisk deep tendon reflexes. Routine MRI sequences showed two types of lesions in both cases: 'punctate' hyperintense lesions on T(2)-weighted images (T(2)WI)/fluid-attenuated inversion recovery (FLAIR) images, hypointense on T(1)-weighted images (T(1)WI) and 'diffuse' white matter lesions, hyperintense on T(2)WI/FLAIR sequences and isointense to hypointense on T(1)WI. All lesions showed no contrast enhancement. Both cases were previously clinically and radiologically diagnosed as multiple sclerosis. There was a strong family history consistent with recurrent infarctions in other family members of both patients. Both cases were later diagnosed as CADASIL by skin biopsy/genetic linkage studies and follow-up. CONCLUSION: The cases showed that CADASIL causes stroke-like episodes in adults and can mimic multiple sclerosis on imaging. Clinical evaluation and MRI findings allow a differentiation of the two entities.

Adult↗
PubMed1989

Neuroepidemiology of human T-lymphotrophic virus type-I-associated tropical spastic paraparesis.

Tropical spastic paraparesis (TSP) is a chronic neurological syndrome of gradual onset involving the pyramidal tracts and upper motor neurons, resulting in weakness and stiffness of the lower extremities, hyperactive tendon reflexes, spasticity, low back pain, and urinary disturbances. Clusters of endemic TSP have been noted in Africa, the Seychelles Islands, Colombia, and the Caribbean. Recently, studies have linked human T-lymphotrophic virus type-I (HTLV-I) with the endemic form of the disease. In Japan a very similar clinical syndrome has been identified as HTLV-I-associated myelopathy and may be a non-tropical version of the same disease. The purpose of the present review is to examine the role HTLV-I may play in the pathogenesis of these myelopathies from a neuroepidemiological point of view.

Adult↗
PubMed1990

Neurological examination in subjects over 65 years: an epidemiological survey.

The frequency of abnormal findings at neurological examination was analyzed in an unselected sample of elderly people aged 67-87 years. Absent deep tendon reflexes and impairment of proprioceptive sensation rarely occurred in the elderly. Limitation of upward gaze and convergence appear a common finding, especially in the very old. Overall, the presence of cortical disinhibition signs (primitive reflexes and paratonia) did not discriminate well between subjects without CNS disease and demented patients. Only the presence of a prominent and persistent response to the stimulus and the number of cortical disinhibition signs found in the same subject appear useful criteria to distinguish between normality and dementia.

Aged↗
PubMed1993

Reversible motor neuron disease.

We investigated a 69-year-old male with a clinical syndrome resembling amyotrophic lateral sclerosis characterized by fasciculation, wasting of the limb muscles and increased deep tendon reflexes in the lower limbs. Electromyographic (EMG) studies showed abundant positive sharp waves and fibrillation potentials with decreased recruitment in the limbs and paraspinal muscles. The patient recovered almost completely in approximately 1.5 years, and follow-up EMG studies showed no positive sharp waves or fibrillation potentials in the limb muscles except for some polyphasic motor units in the bilateral intrinsic hand muscles. No known systemic disease, malignancy or heavy metal intoxication was found during the course of his illness. So far, there are only few cases reported with spontaneous remission of motor neuron disease; however, the possibility should always be considered.

Aged↗
PubMed1996

Development of subtle neurological signs after systemic illness in HIV-infected individuals.

Thirty human immunodeficiency virus (HIV) infected individuals entered a longitudinal study without signs of dysfunction of the central nervous system (CNS). Nine of these individuals developed a systemic illness between study visits, and 7 of these 9 patients (78%) had neurological signs at the next examination (e.g., action-intention tremors, abnormal gait, release signs, abnormal deep tendon reflexes). Only 2/21 (9.5%) of the subjects who did not develop systemic illness showed such signs. These data are consistent with the hypothesis that other factors (e.g. cytokines) as well as the HIV may cause subtle CNS dysfunction.

AIDS Dementia Complex↗
PubMed1990

Functional anatomy of the human saccus lacrimalis.

The relations between the saccus lacrimalis and different portions of the musculus orbicularis oculi were studied in orbital regions of human fetuses sectioned into numbered series. No insertions of the pars lacrimalis or Horner's muscle on the saccus were found. These muscular fibres pass along the dorsal wall of the saccus and are separated from it by the reflex tendon of the ligamentum palpebrale mediale. The only muscular fibres that insert on the saccus are those that approach the anterior face of the saccus and the fornix. The fibres that insert on the anterior face proceed from the deep bundles of the pars preseptalis of the lower eyelids, and those that insert on the fornix derive from the deep bundles of the pars preseptalis of the upper eyelid.

Female↗
PubMed1993

A case of Kearns-Shy syndrome with later onset.

We report a case of Kearns-Shy syndrome in a 44-year-old woman. She complained of bilateral ptosis, exotropia and gait disturbance. Diffuse chorioretinal degeneration and numerous punctate whitish spots were observed in both fundi. Eye movements were severely disturbed. An electroretinogram was almost nonrecordable, while visually evoked cortical potentials to pattern stimulation were normal. The dark adaptation curve showed an elevation of rod threshold. Besides such ophthalmological findings, muscle weakness, extinguished tendon reflex and healing difficulty were observed. Blood lactate, pyruvic acid and serum creatinine kinase were at high levels. A muscle biopsy showed ragged-red fibers and partial deficiency of cytochrome c oxidase. The patient is being treated with coenzyme Q, and we are now following up the therapeutic effects of this treatment.

Adult↗
PubMed1998

A truncated species of apolipoprotein B (B-38.7) in a patient with homozygous hypobetalipoproteinemia associated with diabetes mellitus.

Familial hypobetalipoproteinemia is caused by mutations in the apolipoprotein (apo) B gene. We identified a 57-year-old woman whose plasma total cholesterol and apoB levels were 2.17 mmol/L and 0.03 g/L, respectively. Separation of plasma lipoproteins by sodium dodecyl sulfate-polyacrylamide gel electrophoresis revealed the absence of apoB-100 and the presence of a faster-migrating form of apoB with an apparent Mr of 195 kDa. Direct sequencing of a polymerase chain reaction-amplified fragment of the patient's apoB gene DNA revealed a single C-->T transition at nucleotide 5472 that converts glutamine 1755 (CAA) to a stop codon (TAA). We predict this novel nonsense mutation of the apoB gene to produce a truncated protein that contains 1754 amino-terminal amino acid residues of apoB-100. We designated this mutant form of apoB apoB-38.7 by following the centile nomenclature of the apoB species. The same mutation was found in both of her children. The proband revealed clinical findings of retinitis pigmentosa, acanthocytosis, and loss of deep tendon reflexes that are characteristic of severe hypobetalipoproteinemia. In addition, the proband had type II diabetes mellitus with nephropathy, anemia, cholelithiasis, hepatic hemangioma, bronchiectasis, and extensive calcification of major arteries including, the celiac, splenic, and renal. In summary, we have found a novel truncated apoB, apoB-38.7, in a patient with an unusual presentation of hypobetalipoproteinemia that includes diabetes mellitus and extensive arterial calcification.

Apolipoproteins B↗
PubMed1994

Baseline silent cerebral infarction in the Asymptomatic Carotid Atherosclerosis Study.

BACKGROUND AND PURPOSE: In a group of patients with high-grade asymptomatic carotid artery stenosis, we prospectively determined the prevalence and radiological characteristics of clinically asymptomatic brain infarction evident on computed tomography. Risk factors and extent of carotid disease were also determined. METHODS: Patients randomized into the Asymptomatic Carotid Atherosclerosis Study (ACAS) underwent a neurological history, a detailed stroke/transient ischemic attack questionnaire, and a detailed neurological examination. Computed tomography scans were examined by standardized criteria developed as part of a quality-control program supervised by a neuroradiologist. The presence, location, and size of all cerebral infarctions evident by computed tomography were determined. RESULTS: Among 1132 patients, 848 had no history of stroke or transient ischemic attack. One hundred twenty-six patients (15%) had a silent infarct; 95 (11%) had one, 24 (3%) had two, and 7 (1%) had three or more infarcts. The infarct size was small and deep for 117 patients (72%), less than one-half lobe for 45 (28%), and one-half to less than one lobe for 1 (0.5%). The silent infarcts were evenly distributed ipsilaterally and contralaterally to the study artery but were significantly more frequent in the right hemisphere (P < .05). Factors associated with silent infarction were abnormal gait (P < .001), abnormal deep tendon reflexes or plantar responses (P = .038), but not degree of carotid stenosis. Silent infarction was less frequent among this totally asymptomatic cohort (15%) compared with those with transient ischemic attacks (34/139, 25%; P < .001). CONCLUSIONS: Silent infarction in the setting of asymptomatic carotid stenosis is not uncommon, but silent infarctions are rarely sizable. The clinical significance of silent cerebral infarction in patients with asymptomatic carotid artery stenosis has yet to be established.

Adult↗
PubMed1995

Posterior cerebral artery stenosis with midbrain infarction.

BACKGROUND: Brain infarction secondary to stenosis of the posterior cerebral artery is uncommon. We report a patient with midbrain infarction and symptoms of both Benedikt's and pupil-sparing oculomotor palsy syndromes secondary to posterior cerebral artery stenosis. CASE DESCRIPTION: A 51-year-old woman developed diplopia, left ptosis, and right hemiataxia and hyperactive tendon reflexes. Pupils were equal and reactive. Radiological examination revealed stenosis of the posterior cerebral artery and left-sided midbrain infarct. CONCLUSIONS: Stenosis of the posterior cerebral artery may cause only midbrain infarction and may be responsible for Benedikt's and pupil-sparing oculomotor palsy syndromes.

Brain↗
PubMed1979

Acute triclofos poisoning in a preterm infant.

A preterm infant with accidental triclofos sodium poisoning is described. He developed deep coma, severe hypothermia, mild by hypotension and lack of the primitive and deep tendon reflexes. During recovery, the primitive reflexes were the last to appear. The natural course of triclofos poisoning, and its influence on the immature central nervous system of the preterm infant are discussed.

Central Nervous System↗
PubMed1990

Neurologic complications in chronic renal failure: a retrospective study.

We have retrospectively examined 324 patients with chronic renal failure and evaluated the probable underlying causes of neurologic complications, laboratory data and therapeutic interventions. The common neurologic problems in our patients were alterations in consciousness (40.7%) and convulsions (35.1%). When BUN concentration was above 135 mg/dl and creatinine clearance was below 8 m/min/1.73 m2, alteration of consciousness was observed and when BUN concentration was 200 mg/dl and creatinine clearance was below 7 m/min/1.73 m2, abnormal convulsives appeared. Changes in deep tendon reflexes and pathologic reflexes were associated with hypertension. All of the patients with cortical atrophy using computerized cranial tomography aluminum hydroxide at least for 18 months, and six of them had hemodialysis. Fourteen patients who underwent dialysis developed convulsions and were thought to have disequilibrium syndrome. These findings are consistent with the suggestion that the metabolic and biochemical derangements associated with CRF may be particularly detrimental to the still developing CNS of the child.

Adolescent↗
PubMed1994

Early outcome determination of low-birth-weight infants using the Neurodevelopmental Risk Examination.

A neonatal neurodevelopmental assessment, the Neurodevelopmental Risk Examination (NRE), was developed, through adaptation of the scoring of the Allen/Capute neonatal neurodevelopmental examination, for screening the development of low-birth-weight (LBW) infants in the newborn period. A pilot study was conducted of the NRE and its ability to predict motor and cognitive outcome in LBW infants. The NRE was performed on 92 LBW infants (mean birth weight 1,192 g; mean gestational age 29 weeks) at or near term and included assessments of sensory/behavioral response, axial tone, extremity tone, deep tendon reflexes, and primitive reflexes. Developmental outcome was assessed at a mean age of 13.7 months by neuromotor examination and by the mental scale of the Bayley Scales of Infant Development. The NRE total risk score, reflecting overall neurodevelopmental status, correlated well with motor and cognitive outcomes (r = .50, P = .0001; and r = -.38, P = .0001, respectively). When infants were clustered into risk groups based upon NRE score (69 infants were deemed low-risk, 20 moderate-risk, and three high-risk), a strong relationship to outcome was maintained (motor outcome: chi 2 = 43.6, P < .0001; cognitive outcome: analysis of variance (ANOVA) F = 6.78, df(2.89), P = .002). All subcategories of the examination, except primitive reflexes, were associated with outcome. Therefore, by using a simple method of scoring and interpretation, the NRE can validly predict motor and cognitive outcome in LBW infants.

Cognition↗
PubMed2001

Hypopotassemic paralysis: a rare presentation of proximal renal tubular acidosis.

Neurologic manifestations can accompany systemic diseases, and primary disease can be identified with a careful history, physical examination, and laboratory investigations. A 14-year-old girl with paraplegia and absence of deep tendon reflexes in the lower extremities after 2 days of vomiting and diarrhea was referred to our pediatric neurology department with a diagnosis of Guillain-Barré syndrome. Short stature, dehydration, motor and mental retardation, bilateral cataracts, glaucoma, and band keratopathy were detected on physical examination. Hypopotassemia and severe metabolic acidosis were found on biochemical examination. Her paraplegia improved after appropriate fluid and electrolyte replacement, but metabolic acidosis persisted after cessation of intravenous therapy, and isolated proximal renal tubular acidosis was detected. Because she had isolated proximal renal tubular acidosis and other abnormalities, she was diagnosed with Donckerwolcke-Winsnes syndrome.

Acidosis, Renal Tubular↗
PubMed2003

Central pontine and extrapontine myelinolysis owing to disequilibrium syndrome.

Neurologic disorders can be seen in patients with end-stage renal failure owing to complications of hemodialysis or peritoneal dialysis. The disequilibrium syndrome can be seen, usually soon after or toward the end of dialysis. We report a patient with central pontine and extrapontine myelinolysis owing to disequilibrium syndrome. The patient had depressed consciousness, agitation, tremor, stupor and hyperactive deep tendon reflexes toward the end of the second peritoneal dialysis. A brain computed tomographic (CT) scan showed hypodense lesions in pontine and extrapontine locations without radiocontrast medium enhancement After 2 days, the patient had only minimal memory deficits. A control brain CT scan 1 week later showed a decrease of the lesions in central pontine and extrapontine locations. Central pontine and extrapontine myelinolysis should be suspected and investigated in the acute neurologic disorders of dialysis patients.

Child↗
PubMed2006

Metronidazole: newly recognized cause of autonomic neuropathy.

Metronidazole is a commonly used antibiotic prescribed for the treatment of anaerobic and protozoal infections of the gastrointestinal and genitourinary tracts. It is associated with numerous neurologic complications, including peripheral neuropathy. Neuropathy is typically detected in patients on chronic therapy, although it has been documented in those taking large doses for acute infections. Numerous case reports have been published describing motor and sensory neuropathy, yet autonomic neuropathy has not been described with metronidazole use. A previously healthy 15-year-old girl presented with complaints of burning pain in her feet following a short course of metronidazole for vaginitis. She could obtain pain relief only by submerging her feet in ice water. Examination revealed cold and swollen lower extremities that became erythematous and very warm when removed from the ice water. Temperature perception was reduced to the upper third of the shin bilaterally. Deep tendon reflexes and strength were preserved. Nerve conduction studies demonstrated a peripheral neuropathy manifested by reduced sensory nerve and compound muscle action potentials. Reproducible sympathetic skin potential responses could not be obtained in the hand and foot, providing evidence of a concurrent autonomic neuropathy. A thorough evaluation revealed no other cause for her condition. Repeated nerve conduction studies and sympathetic skin potentials returned to normal over the course of 6 months, paralleling the patient's clinical improvement. Metronidazole is a potential cause of reversible autonomic neuropathy.

Action Potentials↗
PubMed1991

Jitteriness beyond the neonatal period: a benign pattern of movement in infancy.

Jitteriness is a frequent, well-recognized phenomenon in neonates. Its occurrence in early infancy, beyond the neonatal period, is much less documented. Thirty-eight full-term infants who were jittery after 6 weeks of age were followed until the jitteriness disappeared and then reevaluated at the age of 3 years. The jittery movements had already been observed during the neonatal period in 16 babies but not before 6 weeks of age in 22. In 34 infants (89%), 1- and 5-minute Apgar scores were 9 or 10. At the initial examination, a mildly increased muscle tone was found in 12 infants, and hyperactive deep-tendon reflexes were found in 19. The jitteriness resolved at a mean age of 7.2 +/- 3.4 months. At 3 years, 92% of the infants had a normal neurodevelopmental examination, while in the rest only minor, transient disturbances were found. This study indicates that jitteriness as a sole presentation in infants beyond the neonatal period is a benign phenomenon, associated with an excellent prognosis. Its etiology is unknown but seems most likely to be related to a maturational process within the central nervous system.

Apgar Score↗
PubMed1994

Leigh syndrome: pyruvate dehydrogenase defect. A case with peripheral neuropathy.

Pyruvate dehydrogenase deficiency is one of the most common causes of encephalopathy associated with lactic acidosis and is known to account for congenital lactic acidosis, recurrent ataxia, and infantile Leigh syndrome. Hitherto, however, peripheral neuropathy has not been regarded as a presenting symptom of pyruvate dehydrogenase deficiency. Here, we report on a boy who presented peripheral neuropathy with severe limb hypotonia, absent deep-tendon reflexes, and reduced motor nerve conduction velocities at 8 months of age. Persistent hyperpyruvicemia with normal lactate/pyruvate molar ratios in plasma were highly suggestive of a pyruvate dehydrogenase deficiency, and the determination of pyruvate dehydrogenase activity in circulating lymphocytes led to the diagnosis of pyruvate decarboxylase (PDH-E1) deficiency in the proband. Based on this observation, we suggest that pyruvate dehydrogenase deficiency should be considered in the diagnosis of peripheral neuropathy in infancy, especially when associated with persistent hyperpyruvicemia, normal lactate/pyruvate molar ratios in plasma, and recurrent episodes of drowsiness and hypotonia of unknown origin.

Brain↗