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PubMedDate not supplied

Increased serum creatine kinase due to hypocalcemia in vitamin D deficiency.

An 8-year-old boy with vitamin D-deficiency rickets, increased serum creatine kinase (CK), and hypocalcemia is described. At 5 years of age, he was evaluated because of recurrent tonic seizures. He had growth retardation, microcephaly, quadriplegia, mental retardation, and epilepsy. Muscle strength was difficult to assess because of multiple joint contractures. Deep tendon reflexes were hyperactive. Laboratory data indicated rachitic changes on x-ray, hypocalcemia, low serum 25-hydroxyvitamin D3 (25-OH-D) and 1-alpha-25-dihydroxyvitamin D3 (1-alpha-25-[OH]2-D) levels, a normal response to the Ellsworth-Howard test, and markedly increased CK. Electromyography and nerve conduction velocities were normal. The patient responded to 1-alpha-OH-D treatment with increased serum calcium and normal CK activity; a significant correlation (p less than 0.01) was observed between calcium and log CK. The clinical course and laboratory findings supported the hypothesis that the increased CK was due to hypocalcemia, which in turn was due to the vitamin D deficiency in the severely handicapped child with malnutrition.

Alkaline Phosphatase↗
PubMedDate not supplied

Spinal cord birth injury: value of computed tomographic myelography.

The value of myelography in the assessment of spinal cord injury in the early neonatal period has not been documented, although this study has been recommended frequently in the literature. Eight neonates are reviewed who presented with the clinical features of spinal cord injury and who had myelography performed. Clinical features included difficult delivery, absent respiration, flaccid paralysis, sensory level, and neurogenic bladder. Myelography revealed that 7 patients had the early changes of swollen cord and 1 patient had the late changes of cord atrophy. None of the neonates had surgical intervention. One neonate died at 3 days of age, while 2 others died after prolonged ventilation. Of the 5 infants who survived, 3 still require ventilation and have spastic quadriparesis, 1 has almost recovered completely and 1 had spontaneous respiration and limb movement but brisk deep tendon reflexes when last examined at 1 month of age. Myelography, which was performed in the early neonatal period in our infants, was abnormal in all patients. Myelography is useful in confirming the diagnosis, outlining the level and extent of the lesion, and excluding extramedullary compression. Myelography may assist in the assessment of prognosis but did not alter management in our patients.

Birth Injuries↗
PubMedDate not supplied

Nontraumatic spinal intramedullary hemorrhage in an infant.

After an uncomplicated pregnancy and delivery, this female child suddenly became quadriplegic on the fifth day of life. She gradually regained movement in her upper extremities. At 2 months of age, she exhibited paraplegia with exaggerated deep tendon reflexes in the lower extremities. Babinski reflex was present bilaterally and sensory disturbances below the trunk were suspected. Somatosensory evoked potentials after median and ulnar nerve stimulation revealed preserved conduction from the upper extremities through the cervical spinal cord to the cortex. Somatosensory evoked potentials after posterior tibial nerve stimulation suggested disturbed conduction in the upper thoracic spinal cord. Magnetic resonance imaging disclosed a hypodense area in the thoracic cord between T1 and T4 on both the T1-weighted and gradient echo images consonant with an old hematoma cavity. Digital subtraction angiography failed to demonstrate any vascular malformation.

Evoked Potentials, Somatosensory↗
PubMedDate not supplied

Anencephaly: clinical determination of brain death and neuropathologic studies.

Twelve liveborn anencephalic infants were serially examined to determine if they would meet our clinical criteria for whole brain death within a 7-day period: Protocol 1 infants (6) received intensive care including intubation from birth; and Protocol 2 infants (6) received intensive care during the period in which death was imminent. Brain death was determined by absence of brainstem function, including loss of all cranial nerve responses and sustained apnea (PCO2 greater than 60 torr) for 48 hours with confirmation of findings by an outside consulting child neurologist. The initial examinations of these 12 infants revealed spontaneous movements and startle myoclonus (12), suck, root, and gag responses (7), increased tone (8), deep tendon reflexes (9), absent pupillary responses (9), absent oculocephalic and corneal responses (6), absent auditory/Moro responses (7), and nonvisualization of the optic nerve (8). Mild depression of neurologic function occurred during the first several days of life; subsequently, the infants' responses were easier to elicit and more sustained. Only 2 infants met the clinical criteria for brain death. Neuropathologic findings indicated that observed complex motor responses were not based upon cortical activity because no infant had a normally-formed cerebrum. Brainstem neuronal activity may have accounted for these motor responses in some patients but even at this level neurons were scanty or absent. Our findings suggest that, although rare, clinical brain death can be determined in liveborn anencephalic infants; ophthalmologic and otologic developmental abnormalities may confound examination of cranial nerve function; and absence of cortical neurons supports the widely held opinion that these infants do not experience sensation.

Anencephaly↗
PubMedDate not supplied

Pre-eruptive varicella encephalitis and cerebellar ataxia.

Varicella-related neurologic symptoms usually appear during or following the exanthem. Pre-eruptive neurologic manifestations are extremely rare. We report a 6-year-old boy who developed encephalitis, characterized by drowsiness and left-sided hyperactive deep tendon reflexes and cerebellar ataxia, both of which antedated the exanthem by 16 days. The diagnostic and public health implications are discussed.

Antibodies, Viral↗
PubMedDate not supplied

Prospective study of spinal muscular atrophy before age 6 years. DCN/SMA Group.

Spinal muscular atrophy (SMA) is a common neuromuscular disorder of childhood, associated with a high mortality rate during the first 2 years of life. Most practitioners expect patients with SMA to follow a progressive course with loss of muscle strength and function over 2-10 years. Counselling sessions with parents frequently emphasize the high mortality rate and risk for respiratory failure. The progressive nature of SMA has been attributed to the loss of motor neurons. Fifty-eight children, ages 6 years and younger, were examined between January, 1987, and April, 1992, as part of a large, multicenter collaborative study of SMA. Muscle function was evaluated at regular intervals using a standardized protocol that was demonstrated to be reliable. We determined a prevalence of 56% for tongue fasciculations, a prevalence of 22% for facial weakness, and persistent deep tendon reflexes in one patient. Improved motor function and acquired milestones during the study were documented. This work should contribute toward a better understanding of the natural history of SMA.

Child↗
PubMed1995

Muscle involvement in congenital insensitivity to pain with anhidrosis.

A patient with congenital insensitivity to pain with anhidrosis, who had characteristic clinical features and biopsied sural nerve, is presented. Nerve pathology findings indicated a loss of the small myelinated and unmyelinated fibers. Biopsied muscle disclosed a marked variation in fiber size, some small fibers with central nuclei, and a small number of small angulated fibers, consistent with neurogenic and myogenic changes. Many patients with congenital insensitivity to pain with anhidrosis had muscle weakness and absent or decreased deep tendon reflexes with normal nerve conduction velocity. We confirmed that lack of small myelinated fibers in motor neurons resulted in a striking change of muscle in our patient.

Biopsy↗
PubMed1995

Autonomic function in type I diabetes mellitus complicated by nephropathy. A cross-sectional analysis in the presymptomatic phase.

The purpose of this study was to determine the prevalence of parasympathetic and sympathetic autonomic dysfunction in long-standing type I diabetics with established nephropathy and to correlate autonomic function with cardiac risk factors. We used prospective analysis of heart rate variations to standardized testing and 24-hour blood pressure control prior to enrollment in a study utilizing various methods of intense diabetic control to prevent deterioration of kidney function. The settings were outpatient clinical research units. The patients were 42 type I diabetics with proteinuria (total urinary protein > or = 300 mg/day or urinary albumin > or = 100 mg/day) and creatinine clearance > or = 30 mL/min. Heart rate variation during respiratory cycles with change in posture from supine to upright, and during the Valsalva maneuver was recorded by a computerized method. Mean arterial blood pressure was recorded for 24 h by a computerized method. Heart rate variations in this group were abnormal during timed respiratory cycles in 26 of 40 patients (56%), during changes in posture in 15 of 40 patients (38%), and during Valsalva maneuver in 13 of 34 patients (38%) whose retinal disease permitted Valsalva testing. Blunted day/night mean arterial pressure ratios occurred in 18 of 41 (44%) patients and were more severe in men than in women (1.00 v 1.06, P < or = .05). Absence of deep tendon reflexes was associated with an increased incidence of both parasympathetic (respiratory rate variation) and sympathetic (postural rate variation) abnormalities (both P < or = .05). Loss of vibration sensation was not associated with autonomic functional abnormalities.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Neurologic involvement in primary Sjögren's syndrome: a preliminary report.

Forty consecutive patients with primary Sjögren's syndrome (SS) were prospectively evaluated for evidence of neurologic manifestations of the disease. All patients had primary SS diagnosed on the basis of typical sicca symptomatology, objective documentation of keratoconjunctivitis sicca (KCS) and/or xerostomia, and a positive minor labial salivary gland biopsy. None had criteria that would classify him/her as systemic lupus. Evaluation included a detailed neurologic history and physical examination and nerve-conduction studies of all four extremities. Ten patients had a mild sensory or mixed neuropathy of the glove-stocking pattern, and six of them had abnormal nerve conduction studies. Two of those, plus one more, had trigeminal neuropathy. Two more patients had abnormal electrophysiologic studies, one of them with absence of Achilles tendon reflexes as well. None of the above patients volunteered complaints related to these findings. Only one patient with severe primary SS, manifested by cryoglobulinemia, vasculitis and glomerulonephritis, presented with mononeuritis multiplex, that partially responded to intravenous cyclophosphamide and high-dose steroids. Central nervous system (CNS) disease was not detected in any of our patients, suggesting that it is rather rare, whereas peripheral nervous system (PNS) involvement is relatively common and benign in the majority of primary SS individuals.

Autoantibodies↗
PubMed1994

Paclitaxel (Taxol) induces cumulative mild neurotoxicity.

Paclitaxel (Taxol), a new antineoplastic drug, has been reported to be neurotoxic at doses above 200 mg/m2 per course. It is uncertain whether neurotoxicity is related to cumulative amounts of paclitaxel. Neuropathy was prospectively assessed in 18 patients with breast cancer, receiving between two and eight courses of 135 or 175 mg/m2 of paclitaxel. Vibratory perception thresholds (VPT) and tendon reflex scores were proportionally related to the corresponding cumulative amounts of paclitaxel (P = 0.002; P = 0.0003). The amounts of paclitaxel administered between the first and last assessments (175-1225 mg/m2) were related to concomitant changes in VPT (P = 0.034). Paclitaxel had no clear neurotoxic threshold; if present, it lies below 540 mg/m2. Rather, VPT appeared to increase 0.1 micron per 400 mg/m2 over the entire range of 175-1225 mg/m2 of paclitaxel. Clinical neuropathy prevailed in 0/8 patients at screening and in 5/10 patients at the final assessment (P = 0.029). Neuropathy never exceeded grade 1. Thus, although neurotoxicity of paclitaxel is frequent and cumulative, it remains mild or subclinical up to at least 1400 mg/m2 administered over eight cycles.

Adult↗
PubMed2004

Eosinophilic meningitis in a child raising snails as pets.

The rat lungworm (Angiostrongylus cantonensis) is the principal cause of eosinophilic meningitis or meningoencephalitis worldwide. It is endemic in Taiwan and the Asia Pacific area. We report the case of a 10-year-old boy who was referred to us suffering from intermittent headache, low-grade fever and blurred vision of 4-5 days' duration. He had been treated for gastroenteritis just prior to referral. The patient's history was unremarkable, except that he raised snail (Ampullarium canaliculatus) as pet at home. On physical examination, the patient's consciousness was alert and well oriented. No papilledema was found on fundal examination. The neurological examination revealed normal cranial nerve function, mild weakness of both lower limbs and normal deep tendon reflexes, but positive Babinski and Kernig signs. Laboratory findings showed peripheral eosinophilia, elevated immunoglobulin E level, cerebrospinal fluid eosinophilic pleocytosis and the presence of stage 3 A. cantonensis larvae, which confirmed the diagnosis of eosinophilic meningitis. A 2-week course of mebendazole combined the glucocorticosteroids was beneficial in relieving headache, paresthesia and the other eosinophilic meningitis symptoms in the patient.

Angiostrongylus cantonensis↗
PubMed2005

A pediatric case of critical illness polyneuropathy: clinical and pathological findings.

Critical illness polyneuropathy (CIP) is a sensorimotor polyneuropathy recognized in adult intensive care patients with sepsis and multiple organ dysfunction and only a few cases have been reported in children. Here we report a 13-year-old Japanese boy with CIP that developed during the course of encephalopathy. Two months after the onset of encephalopathy, he developed tetraplegia although consciousness had already recovered. Deep tendon reflex was absent. MRI of the brain and spinal cord was normal and no abnormality in the cerebrospinal fluid was detected. Motor and sensory nerve conduction velocities of the lower limbs and somatosensory evoked potential could not be detected. The motor activity subsequently showed gradual recovery, although standing and walking could not be achieved. Sural nerve biopsy performed 3 years after the onset showed severe reduction of the number of myelinated large-diameter fibers, thin myelin in almost all fibers and cluster formation of myelinated small-diameter fibers, indicating primary axonal degeneration with regeneration. We report here for the first time the neuropathological changes in peripheral nerves during the chronic stage of CIP in children.

Adolescent↗
PubMed2005

Bilateral brachial plexopathy complicating Henoch-Schönlein purpura.

An 11-year-old boy presented with convulsion, fever, rash, abdominal pain, swelling on the eyelids, elbow and wrists, oliguria and hematuria. Based on the abnormal findings the patient was diagnosed with Henoch-Schönlein purpura. On the 3rd day of admission, neurological examination showed ataxic gait, loss of deep tendon reflexes, and decreased (4/5) of muscle strength on all extremities. Additionally, bilateral loss of touch, pain and temperature sensation in a glove, from the elbows to distal region (on C5-T1 level) was diagnosed. Cerebrospinal fluid examination and cranial magnetic resonance imaging (MRI) were normal. The patient was discharged with oral prednisolone on the 7th day of admission. One week after discharging from the hospital, he was re-admitted with vertigo and seizures. He was in coma. MRI of cranial, cervical and cervical plexus were normal. Electromyography showed severe bilateral brachial plexopathy. Prednisolone and intravenous immunglobulin (IVIG) therapy were given without significant improvement. He was discharged from the hospital on the 17th day of admission. On the second month of follow-up, a second cure of IVIG was given because of no clinical improvement. Now, he is on the 4th month of follow-up, unfortunately, no improvement was noted on his muscle strength and sensorial abnormalities on the upper extremities.

Brachial Plexus Neuropathies↗
PubMed2006

Isolated Dandy-Walker malformation associated with brain stem dysgenesis in male sibs.

We describe two brothers with isolated Dandy-Walker malformation (DWM). Interestingly, brain stem dysgenesis and abnormal gyral pattern were also observed in the sibs. They presented with psychomotor retardation and macrocrania. Both suffered from hypotonia with brisk deep tendon reflexes and ataxic gait. They had bilateral optic atrophy and the visual evoked potentials documented prolonged latencies. Further, motor and sensory conduction velocities were normal. Chromosomal examinations for the sibs and their parents showed normal results. The majority of cases are sporadic but rare reports of recurrence in siblings exist. The parents' consanguinity and the recurrence in a subsequent pregnancy suggest an autosomal recessive inheritance pattern. Our report adds more weight that brain stem dysgenesis could be associated with DWM, increasing the spectrum of heterogeneity of this malformation.

Brain Stem↗
PubMed2005

Mitochondrial neuropathy.

Polyneuropathy is a frequent feature of mitochondriopathy (MCP). If and how often polyneuropathy in MCP is primarily due to the underlying disorder (mitochondrial neuropathy, MN) or due to other well-known causes is unknown. Retrospectively investigated were 108 MCP-patients with polyneuropathy. According to established diagnostic criteria 37 patients were classified as definite MCP, 56 as probable MCP and 15 as possible MCP. In 38 of the 108 MCP-patients with polyneuropathy (35%), no plausible cause for polyneuropathy other than MCP could be found. MN was characterized by weakness, muscle cramps, wasting, reduced tendon reflexes, muscle pain, ataxia, restless legs, hypesthesia, paresthesia, dysesthesia, and vegetative impairment. In 21 cases predominantly motor fibers, in 14 cases both motor and sensory fibers and in 3 cases predominantly sensory fibers were affected. Axonal degeneration was found in 19 cases, demyelination in 4 and mixed-type polyneuropathy in 15. On sural nerve biopsy axonal loss was the predominant finding. In a single case tomaculae and abnormally shaped and structured mitochondria were found. MN exists, occurs in one third of the MCP-patients with polyneuropathy, and is characterized by predominant affection of the motor and sensory fibers with diffuse, symmetric and equal distribution between upper and lower limbs and by axonal degeneration.

Adult↗
PubMed2005

A case of late-onset Segawa syndrome (autosomal dominant dopa-responsive dystonia) with a novel mutation of the GTP-cyclohydrase I (GCH1) gene.

We report a case of a 46-year-old Japanese woman with hereditary progressive dystonia with marked diurnal fluctuations and dopa-responsive dystonia (HPD/DRD). She developed difficulty in walking at the age of 44 years due to bradykinesia as well as hand tremors, muscle rigidity, increased tendon reflexes and mild dystonia in the lower extremities, all of which responded remarkably to low doses of levodopa (150 mg/day). Biopterin and neopterin concentrations in the cerebrospinal fluid (CSF) were decreased. Analysis of the guanosine 5'-triphosphate cyclohydrolase I (GCH1) gene revealed a novel mutation (W53X) in one allele. The GCH1 activity that was expressed in mononuclear blood cells was almost half the normal value (usually 2-20% of the normal value (39.0+/-9.2 pmol/ml) in patients with HPD/DRD). The relatively conserved GCH1 activity that is expressed in stimulated peripheral blood mononuclear cells may be related to the late clinical symptoms in this patient.

Biopterins↗
PubMed2006

Recurrent limbic and extralimbic encephalitis associated with thymoma.

A 33-year-old woman, with a 7-year clinical history of invasive thymoma treated at ages 26 and 30 years by thymectomy and radiation, presented with a generalized convulsion and loss of consciousness. Following the seizure there was no neurological deficit and normal tendon reflexes. Magnetic resonance imaging (MRI) of the brain without gadolinium enhancement revealed multiple small lesions of high signal intensity on T2 and diffusion weighted images located in the cortical area beyond the temporal lobes. Brain biopsy demonstrated encephalitis with activated microglias and activated T-cell infiltration. Within 4 months of treatment with nothing other than anticonvulsant therapy, the lesions visible on the original MRI had completely disappeared and the patient was discharged with no neurological symptoms. The patient subsequently had two more episodes with a variety of symptoms such as incontinence, confusion, aphasia, apallial syndrome, and motor paresis. MRI following these episodes again revealed multiple lesions of similar appearance to those of the first episode, although in different locations, and much larger and more numerous. The patient had steroid pulse therapy after both episodes and the lesions noted on brain MRI disappeared within a few months with minimal neurological complications.

Administration, Oral↗
PubMed2004

Neurological and cognitive impairment associated with leaded gasoline encephalopathy.

BACKGROUND: A toxic encephalopathy (or 'lead encephalopathy') may arise from leaded gasoline abuse that is characterised by tremor, hallucinations, nystagmus, ataxia, seizures and death. This syndrome requires emergency and intensive hospital treatment. METHODS: We compared neurological and cognitive function between chronic gasoline abusers with (n=15) and without (n=15) a history of leaded gasoline encephalopathy, and with controls who had never abused gasoline (n=15). RESULTS: Both groups of chronic gasoline abusers had abused gasoline for the same length of time and compared to controls, showed equivalently elevated blood lead levels and cognitive abnormalities in the areas of visuo-spatial attention, recognition memory and paired associate learning. However, where gasoline abusers with no history of leaded gasoline encephalopathy showed only mild movement abnormalities, gasoline abusers with a history of leaded gasoline encephalopathy showed severe neurological impairment that manifest as higher rates of gait ataxia, abnormal rapid finger tapping, finger to nose movements, dysdiadochokinesia and heel to knee movements, increased deep tendon reflexes and presence of a palmomental reflex. CONCLUSIONS: While neurological and cognitive functions are disrupted by chronic gasoline abuse, leaded gasoline encephalopathy is associated with additional and long-lasting damage to cortical and cerebellar functions.

Administration, Inhalation↗