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PubMed2006

[Transverse myelitis revealing Hodgkin disease].

INTRODUCTION: Neurological complications during Hodgkin disease are rare and sometimes difficult to diagnose. We report the case of a patient with transverse myelitis. CASE: This 32-year-old man was hospitalized on month after onset of febrile spastic paraplegia, which was accompanied by progressive deterioration of his general condition. Examination revealed a febrile, conscious patient, with abolition of the lower-limb tendon reflexes, bilateral Babinski signs, and sensitivity at D6-D7. We also noted hepatosplenomegaly, but no peripheral adenopathies. Laboratory reports indicated bicytopenia, a major inflammatory syndrome and hepatic cytolysis. The computed tomography examination of thorax and abdomen showed swelling in deep lymph nodes and the brain MRI showed what appeared to be transverse myelitis. The brainstem biopsy was normal; the hepatic biopsy showed liver infiltration by Sternberg cells. The patient died rapidly, before treatment could begin. DISCUSSION: The variable neurological events observed during Hodgkin disease may serve to reveal this disease. Their association with a tumor suggests this diagnosis even when the neurological signs are nonspecific. They may affect either the brain or the brainstem. Diagnostic certainty requires histologic analysis, and prognosis depends on early diagnosis and management.

Adult↗
PubMed1993

The clinical diagnosis of lumbar radiculopathy.

Lumbar radiculopathy may be caused by, or confused with, many different conditions. The nature of the patient's pain--its quality, intensity, location, and profile over time--is an important guide in the evaluation. A careful but directed physical examination is necessary for the clinical evaluation of patients with lumbar spine disease. Evaluation involves inspection of the back and limbs, palpation, and observation of the patient. A careful neurological evaluation, examination of strength, deep tendon reflexes, sensation, and muscular function is necessary. Electromyography is often useful. The most commonly involved nerve roots are L3, L4, L5, and S1. Lesions of each produce distinct symptoms, and other conditions can mimic the radiculopathies. Specific investigation is necessary for an accurate diagnosis.

Electromyography↗
PubMed2002

Osteoid osteoma presenting with focal neurologic signs.

Osteoid osteomas are benign bone tumors, most commonly located in the femur or tibia. In young children, these tumors can be extremely difficult to diagnose. They commonly present nonspecifically with gait disturbance and pain and characteristically respond well to mild pain relievers. We report two patients who presented with neurologic signs, including atrophy, weakness, and diminished deep tendon reflexes of the affected limb. These two patients demonstrate that osteoid osteomas of the lower extremities can present with neurologic signs, and proper diagnosis requires a detailed history and clinical awareness of this phenomenon.

Bone Neoplasms↗
PubMed2003

Miller Fisher syndrome with negative anti-GQ1b immunoglobulin G antibodies.

Miller Fisher syndrome is characterized by a triad of ataxia, ophthalmoplegia, and reduced or absent tendon reflexes, with minimal if any limb weakness. Anti-GQ1b immunoglobulin G antibodies are present in high titers in most patients. Presented is a two-year-old female with Miller Fisher syndrome whose blood serum was negative for anti-GQ1b immunoglobulin G antibodies.

Child, Preschool↗
PubMed1997

Familial Dandy-Walker malformation and leukodystrophy.

We report the first familial cases with two different types of posterior fossa cystic malformation and a leukodystrophic-like aspect on cerebral magnetic resonance imaging (MRI). The girl and her brother had severe encephalopathy, marked hypotonia, absent deep tendon reflexes, macrocrania, gigantism, and dysmorphic face and extremities. The girl had generalized seizures. The boy had unilateral cataract and bilateral optic atrophy. The parents were first cousins, suggesting autosomal recessive transmission. MRI showed Dandy-Walker variant in the girl, with cerebellar vermis hypoplasia and expansion of the cisterna magna, which communicated with the fourth ventricle. Her brother had mega cisterna magna communicating with the fourth ventricle and a normal cerebellum. The 2 children had abnormally high signal in the supratentorial white matter. Visual and auditory evoked potentials revealed prolonged latencies. Motor and sensory conduction velocities were normal. Muscle and nerve biopsies were normal. Metabolic exploration demonstrated no abnormality.

Brain Diseases↗
PubMed2000

Clinical and cerebral FDG PET scan in a patient with Krabbe's disease.

A 2-year, 6-month-old Saudi male with infantile Krabbe's disease was studied with fluorine-18-labeled-2-fluoro-2-deoxyglucose positron emission tomography (FDG PET) scan. The patient presented with a gradual loss of developmental milestones, irritability, and crying. At the advanced stage of the disease, he developed tonic-clonic seizures and became a microcephalic, extremely irritable, blind, spastic quadriplegic child, with no deep tendon reflexes. Laboratory studies revealed normal blood chemistry, muscle enzymes, very long chain fatty acids, and acylcarnitines. No abnormal urinary organic acids were detected. The cerebrospinal fluid protein concentration was increased. Magnetic resonance imaging of the brain revealed mild brain atrophy and white matter disease mainly in the centrum semiovale. Electroretinography was normal; however, electroencephalography and visual-evoked potentials were abnormal. Peripheral nerve conduction studies documented a demyelinating neuropathic process. The FDG PET study of the brain demonstrated a marked decrease in the metabolism of the left cerebral cortex and no uptake in the caudate heads. Normal glucose uptake was observed in the thalami, lentiform nuclei, and cerebellum. The patient did not present for subsequent clinic visits and is presumed dead.

Child, Preschool↗
PubMed1998

Chronic symmetric symptomatic polyneuropathy in the elderly: a field screening investigation of risk factors for polyneuropathy in two Italian communities. Italian General Practitioner Study Group (IGPST).

A total of 4191 patients 55 years and older were screened for clinical features and risk factors of polyneuropathy by 27 general practitioners (GPs) in two areas of Italy (Varese and San Giovanni Rotondo). Polyneuropathy was diagnosed in the presence of two or more symptoms associated with bilateral impairment of at least two of the following: strength, sensation, tendon reflexes. A risk factor for polyneuropathy (associated disease or neurotoxic agent) was recorded based on its presence in the GP's records, the presence of specific treatments, or an affirmative answer to the interviewer's question. The prevalence of polyneuropathy among patients with no recognized exposure to diseases or neurotoxic agents was 1.6% (Varese 1.6%; San Giovanni Rotondo 1.8%). The corresponding values were 11.8% (Varese 11.8%; San Giovanni Rotondo 11.9%) for patients with one risk factor, and 17.3% (Varese 19.2%; San Giovanni Rotondo 13.0%) for patients with two risk factors. Combining the two populations, the prevalence of polyneuropathy was highest in diabetics (18.3%), followed by patients with a diagnosis of alcoholism (12.5%), non-alcoholic liver disease (10.9%), and tumor (7.1%). Diabetes was the commonest independent risk factor for polyneuropathy (odds ratio 11.3), followed by alcoholism (7.4), non-alcoholic liver disease (4.9), and tumor (2.6).

Aged↗
PubMed1997

[Angiostrongylosis in infants in Reunion and Mayotte. Apropos of 3 cases of eosinophilic meningitis including 1 fatal radiculo-myeloencephalitis with hydrocephalus].

BACKGROUND: Eosinophilic meningitis caused by Angiostrongylus cantonensis is widespread in Southeast Asia and Pacific islands. Adults develop a transient meningitis with a benign course but severe or fatal disease may occur in pediatric patients. CASE REPORT: Case 1. A 11-month-old boy living in Mayotte island was hospitalized a few days with fever and skin rash following by seizure, coma, flaccid quadraplegia, absence of deep tendon reflexes, urinary retention and anal incontinence. Eosinophilia was observed in peripheral blood and cerebrospinal fluid. He further developed a triventricular hydrocephalus treated by ventriculoperitoneal shunt. The child died 3 weeks later. A serodiagnosis of angiostrongylus infestation was restrospectively established. Case reports 2 and 3.-Two infants, 10 and 11-month-old-boys, living in Reunion island, developed fever and vomitings, irritability and, for one of them, unilateral sixth cranial nerve palsy. There was eosinophilia in the peripheral blood and in the cerebrospinal fluid. All symptoms progressively disappeared with complete recovery. The suspected diagnosis of angiostrongylus infestation was confirmed by the serology. CONCLUSION: We report the first case of Angiostrongylus cantonensis infection in the French island of Mayone (Comoro Islands) and we confirm the presence of this disease in Reunion island. In this Indian Ocean area, eosinophilic meningitis occurs most of the time in infants with sometimes severe radiculomyeloencephalitic forms.

Angiostrongylus cantonensis↗
PubMed1997

[Smith-Magenis syndrome].

BACKGROUND: The main features of the Smith-Magenis syndrome include broad flat midface, brachycephaly, broad nasal bridge, brachydactyly, hoarse deep voice, speech and developmental delay, and behavioral anomalies. This syndrome is due to interstitial deletion of chromosome 17p11.2. CASE REPORT: A 7-year-old girl was admitted for mental retardation. Clinical examination showed brachycephaly, broad flat midface, broad nasal bridge, malar hypoplasia, brachydactyly, decreased or absent deep tendon reflexes, and hoarse deep voice. She had a mild deafness, behavioral problems, and sleep disturbances. Chromosome analysis on lymphocytes identified a microdeletion of one chromosome subband 17p11.2. Molecular studies indicated loss of maternal allele. CONCLUSION: The Smith-Magenis syndrome is probably underdiagnosed because of its usually mild clinical features. High-resolution chromosome analysis is needed for diagnosis.

Abnormalities, Multiple↗
PubMed1997

Neurological monitoring of neurotoxicity induced by paclitaxel/cisplatin chemotherapy.

To evaluate the neurotoxicity of paclitaxel/cisplatin chemotherapy, we studied neurological and electrophysiological functions in 14 patients who had been treated with 1-7 courses of paclitaxel/cisplatin. The cumulative paclitaxel and cisplatin doses ranged from 175 to 1225 mg/m2 and 100-700 mg/m2, respectively. Neurological examinations as well as motor nerve conduction studies of the peroneal nerve were performed and summarised by means of a peripheral neuropathy score. Neurotoxicity with onset usually after the second treatment cycle occurred in 13 patients. 12 patients complained about sensory symptoms, 13 patients had impaired vibration sense and 8 patients developed additional muscle weakness, predominantly of the legs. Dysfunction of peroneal motor nerve conduction occurred in 13 patients. Reduction of amplitudes as well as slowing of conduction velocities were seen in 13 patients and prolonged distal latencies in 10 patients. The peripheral neuropathy score was elevated in 13 patients. Neurological symptoms, impairment of both vibration sense and tendon reflexes, and the peripheral neuropathy score increased with the cumulative doses of paclitaxel/cisplatin. Serial analysis among selected patients also revealed an increase in neurotoxicity with increasing cumulative drug doses. These data indicate the development of neurotoxicity in most patients treated with paclitaxel/cisplatin and also suggest that early signs of neurotoxicity can be detected by clinical examination with emphasis on symptoms as well as vibration sense and can be well documented by electrophysiological investigations.

Adult↗
PubMed2001

Primary beta-sarcoglycanopathy manifesting as recurrent exercise-induced myoglobinuria.

We report an unusual presentation of a primary beta-sarcoglycanopathy (LGMD type 2E). A 12- year-old boy came to our attention after six episodes of exercise-induced myoglobinuria. Electromyogram showed mild myopathic features of the proximal lower limb muscles. Electrocardiogram was normal. Neurological examination revealed normal muscle strength and reduced deep tendon reflexes. A muscle biopsy showed rare regenerating fibers; the immunohistochemistry was normal for dystrophin, while all the sarcoglycans were diffusely decreased. Western blot analysis showed a relevant decrease of all sarcoglycan proteins and a mild dystrophin reduction. beta-Sarcoglycan gene analysis demonstrated a compound heterozygous status for these mutations: a novel A-T base pair substitution at nucleotide 85 in exon 2, changing the codon Arg to a stop codon; a C-T base pair substitution at nucleotide 272 in exon 3 changing a Arg to a Cys residue. We consider that exercise-induced myoglobinuria may be the presenting sign of primary beta-sarcoglycanopathy.

Base Sequence↗
PubMed2003

Hereditary neuropathy with liability to pressure palsies (HNPP) in a toddler presenting with toe-walking, pain and stiffness.

The typical clinical presentation of hereditary neuropathy with liability to pressure palsies is an adult-onset recurrent, painless monoparesis. Electrophysiological abnormalities--decreased nerve conduction velocities and delayed distal latencies--can be detected even in asymptomatic patients. We describe a toddler, who presented with asymmetric toe walking, painful cramps and stiffness in the legs. He had calf hypertrophy, brisk tendon reflexes and bilateral Babinski signs and the electrophysiological examination was normal. The unlikely diagnosis of hereditary neuropathy with liability to pressure palsies was reached 5 years later, when the boy started to complain of episodic numbness and weakness in the upper extremities. His father, paternal aunt and grandmother had similar symptoms, but they had never been investigated. The typical 1.5 Mb deletion on chromosome 17p11.2-12 was found in our patient and his affected relatives.

Child↗
PubMed1992

Age-dependent axonal loss in nerve biopsy of patients with xeroderma pigmentosum.

We describe the histomorphometric changes in the superficial peroneal nerve biopsy from 13 patients with xeroderma pigmentosum (XP). The mean age at time of biopsy was 15 yr (range 2.5-24 yr). The clinical examination was normal in the two youngest patients and showed absence of the deep tendon reflexes, with choreo-athetosis in ten patients. In addition, in the three oldest patients there were cerebellar signs, ataxia and Babinski signs. The nerve biopsy showed an age-dependent decrease of myelinated fibres, which was mild in the youngest and severe in the oldest patients. This was associated with rare acute axonal degeneration, sparse axonal regeneration, rare axonal atrophy and few onion bulb formations. These findings suggest a neuropathic process. This neuronal degeneration seems to be a progressive and stereotyped phenomenon in XP.

Adolescent↗
PubMed1999

Congenital muscular dystrophy with central and peripheral nervous system involvement in a Belgian patient.

We report a patient with congenital muscular dystrophy (CMD), developmental brain defects, and peripheral neuropathy. Marked hypotonia and plagiocephaly were noted at birth. Failure to thrive, generalized muscle weakness and wasting, absent deep tendon reflexes, partial seizures, and secondary microcephaly developed. Brain MRI showed a large area of cortical dysplasia, a thin but complete corpus callosum, and diffuse ventriculomegaly. Nerve conduction velocities were slow and creatine kinase levels only mildly elevated. Muscle biopsy showed dystrophic features with normal merosin, sarcoglycan, and dystrophin immunostaining. The Japanese Fukuyama CMD founder mutation was not detected. This is the first report of a patient with merosin-positive CMD, cobblestone lissencephaly, and demyelinating peripheral neuropathy.

Atrophy↗
PubMed2003

A case of mucopolysaccharidosis IV with lower leg paresis due to thoraco-lumbar kyphoscoliosis.

We treated a patient of type IV mucopolysaccharidosis (Morquio's disease) with lower leg paresis due to kyphoscoliosis. A 65-year-old woman presented with Morquio's disease. A lateral radiograph demonstrated the classic bullet-shaped vertebrae and a 65 degrees thoraco-lumbar kyphosis. After the age of 60, she suffered from numbness in both lower legs and walking disturbance. Bilateral patellae-tendon reflexes were exaggerated. MRI showed compression of the spinal cord around T12 to L2 with a highlighted area of change inside the spinal cord. Myelography and computed tomography after the myelography showed narrowing of the sub-arachnoidal space and deformation of the spinal cord around the T12 to L2 levels. Severe vertebral osteoporosis made it necessary to first perform posterior correction of the kyphosis and fusion. The curve was stabilised with the Luque method from T7 to L4. Her neurological condition markedly recovered, but 1 year after surgery her neurological condition again began to deteriorate, resulting in walking disturbance. For this reason, anterior decompression and fusion through a lateral thoracotomy was undertaken. Decompression of the spinal cord and a bone graft from the iliac crest were attained. The patient's neurological condition again improved, but not as much as immediately after the first operation.

Aged↗
PubMed2003

Sensorimotor polyneuropathy with 5-aminosalicylic acid: a case report.

A 69-year-old man with ulcerative colitis (UC) developed sensorimotor polyneuropathy. First, he received salazosulphapyridine (SASP) as treatment for the UC. The symptoms of UC disappeared immediately, but he developed skin eruptions and dysesthesia in his lower limbs. When SASP was changed to 5-aminosalicylic acid (5-ASA), his skin eruptions were resolved, however, he developed weakness and atrophy in his right arm as well as progressive worsening of the dysesthesia in his legs and gait disturbance. Deep tendon reflexes (DTR) were absent in all extremities. After 5-ASA was discontinued, the polyneuropathy symptoms recovered gradually. This clinical course suggests that the sensorimotor polyneuropathy may have been caused by 5-ASA.

Aged↗
PubMed1998

Effects of magnesium sulfate tocolysis on maternal mental status.

Objective: Magnesium sulfate is the most commonly used agent for tocolysis in the management of preterm labor. Anecdotally both clinicians and patients have noted alterations in mental status of women receiving high doses of magnesium infusion, and central nervous system depression including lethargy and depression of deep tendon reflexes has been documented. Our hypothesis is that intravenous magnesium sulfate at tocolytic doses significantly affects maternal mental status.Materials and Methods: Eligibility criteria included admission or transport to University Hospital between 25 and 34 weeks gestation with an initial episode of spontaneous premature labor. Patients were consented and given an initial mental status examination prior to magnesium sulfate infusion. Those patients transported to University Hospital diagnosed with premature labor and already on magnesium were consented and given an initial mental status examination at the time of arrival. Once a therapeutic level of magnesium was documented a repeat mental status examination was performed, with a third examination performed 24 hours after the magnesium infusion has been discontinued. As a control group pregnant women hospitalized for premature rupture of the membranes not in labor had the examinations performed initially, after 24 hours of hospitalization, and again after 72 hours of hospitalization. Exclusion criteria included underlying mental illness, administration of other medications that might affect mental status, cervical dilation greater than 4 cm, clinical evidence of chorioamnionitis, or the presence of any significant abnormalities in the fetal heart rate tracing. The mental status examination consisted of the mini mental state exam, the comprehension portion of the Wechsler Adult Intelligence Scale, and the Bender-Gestalt Indicator. The results of these examinations were scored in a blinded fashion by a psychiatrist.Results: There were 22 patients in the study group and 9 patients in the control group. There were no differences in the age, gravidity, parity, or gestational age of the two groups. Out of a possible 102 points, the mean mental status scores were as follows:The mean serum magnesium level at the time of therapy was 5.1 mg/dL. The time required for response to the Wechsler test was significantly different although the scoring of the comprehension was unchanged (15.2 +/- 3.6 min vs 22.3 +/- 4.7 min, P <.05).Conclusions: This prospective blinded study reveals no differences in maternal mental status during magnesium sulfate infusion at the levels recorded in our study. There was an increase in the length of time required to answer the comprehension and judgment portion of the examination. These findings have significant clinical implications suggesting that patients on magnesium sulfate can make appropriate judgments and can, therefore, participate in clinical discussions and trials.

Journal Article↗
PubMed1999

Cauda equina syndrome due to lumbosacral arachnoid cysts in children.

We describe the clinical, neuroradiological and surgical aspects of two children in whom symptoms attributable to cauda equina compression were caused by spinal arachnoid cysts. The first patient presented with recurrent urinary tract infections due to neurogenic bladder dysfunction, absent deep tendon reflexes and sensory deficit in the lower limbs. The second child presented with unstable gait as a result of weakness and diminished sensation in the lower extremities. Spinal magnetic resonance imaging revealed a lumbosacral arachnoid cyst in both patients. During surgery the cysts were identified and excised. Two years after surgery, the sensory deficits of the first patient have disappeared and patellar and ankle reflexes can be elicited, but there is no improvement in bladder function. Neurological examination of the second patient was normal. We conclude that the diagnosis of cauda equina syndrome should prompt a vigorous search for its aetiology. Lumbosacral arachnoid cysts are a rare cause of cauda equina syndrome in children.

Arachnoid Cysts↗