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PubMed2001

A questionnaire for neurological symptoms in patients with diabetes--cross-sectional multicenter study in Saitama Prefecture, Japan.

This study was designed to investigate the prevalence of neurological symptoms in diabetic patients living in Saitama Prefecture, Japan using 13-item questionnaire. A total of 6472 outpatients with diabetes (3417 men and 3055 women) were recruited from 100 centers. Mean age and mean disease duration were 60.9-year old and 10.4 years, respectively. The questionnaire for monitoring of neurological symptoms was completed at the clinic or hospital visited, and Achilles' tendon reflex, ophthalmologic, blood and urinary examinations were also performed. Of the 6472 patients, 84.8% suffered from a mean of 3.3+/-2.2 neurological symptoms. However, half of these symptoms were not considered to be those of diabetic neuropathy by attending physicians. "Feeling as if a piece of paper is attached to the sole of the foot," "stinging and prickling sensations in feet," and "pain in feet" were the most common symptoms of diabetic neuropathy. The prevalence of diabetic neuropathy as determined by attending physician increased with disease duration and worse control of diabetes. This study found that the majority of diabetics were suffered from neurological symptoms, although half of such symptoms were not considered to be those of diabetic neuropathy by physicians. Furthermore, it is important for diabetics to be diagnosed and treated earlier to prevent progression to severe neuropathic complications by means of optimal glycemic control and use of some chemicals such as aldose reductase inhibitor, and to develop this study to evaluate the efficacy of treatments.

Aged↗
PubMed1985

Multiple organ failure resulting from intravenous abuse of methylphenidate hydrochloride.

A 32-year-old woman who abused methylphenidate hydrochloride developed complications including hepatic, renal, pancreatic, pulmonary, and CNS toxicities. These were manifested by abnormal liver function enzymes, poor urine output, hypotension, tachypnea, tachycardia, abnormal blood gases, rising serum BUN and creatinine, and hyperactive deep-tendon reflexes. All were reversible with medication withdrawal and supportive therapy. Toxicities of this medication and their implications are discussed.

Adult↗
PubMed1984

[Lambert-Eaton syndrome. Diagnostic, nosologic and therapeutic problems].

We report on five cases of this myasthenic disorder associated with a loss of deep tendon reflexes, dry mouth and impotence. The diagnosis relies upon the response to repeated electric stimulations: with stimulations at a frequency of 5 Hz, the size of the potentials decreases by more than 30 p. 100 and, at 30 Hz, increases by more than 60 p. 100. This profile differentiates Lambert-Eaton syndrome from myasthenia gravis. Lambert-Eaton syndrome occurs usually in the course of malignant diseases; when it seems isolated, a visceral neoplasm, mainly bronchogenic carcinoma, should be suspected. Nevertheless, in some cases, no malignant disease is found. The mechanism is a presynaptic block of neuromuscular transmission because of an unknown hypothetic substance produced by the tumor. Therapeutic resources (Guanidine) are scarce.

Aged↗
PubMed2001

Massive intravenous immunoglobulin treatment in pregnancy complicated by Guillain-Barré Syndrome.

A pregnant woman developed acute demyelinating poly-neuropathy (Guillain-Barré syndrome (GBS)) in the 28th week of gestation (GW) after flu-like infection. Hypertension, liver dysfunction, and a decrease in consciousness level developed at 29GW. Blood chemical analysis revealed increased levels of liver enzymes GOT 247 IU/l and GPT 624 IU/l. Viral serological study showed a positive test for Epstein-Barr virus IgM. Weakness of bilateral facial muscles and limbs, a loss of tendon reflexes, and generalized paresthesia were detected by neurologic examinations. Over the course of 5 days, a massive dose (100g) of intravenous immunoglobulin (MIVIg) was infused in 30GW. An average manual muscle testing score by the Medical Research Council method and peak flow value began to be significantly restored during and after MIVIg infusions. Values of the liver enzymes gradually decreased, and improvement of the muscle weakness and dysbasia was observed. Her pregnancy normally ended in spontaneous vaginal delivery of a healthy infant in 37GW. This is the first report confirming the efficacy of MIVIg, without plasmapheresis, in GBS-complicated pregnancy.

Adult↗
PubMed2000

Lower motor neuron disease associated with myelofibrosis.

We present a patient who has signs pointing to the involvement of lower motor neurons and myelofibrosis. To our knowledge, unlike lymphoproliferative disorders, co-occurrence of myelofibrosis and lower motor neuron disease (MND) has not been reported so far. A 64-year-old male patient was admitted to our hospital with the complaint of painful cramps in his neck and forearms. On physical examination marked hepatomegaly and splenomegaly were found. On neurologic examination nasal quality of the voice and slight palatal weakness were detected. There were generalised slight weakness and atrophy in both proximal and distal muscle groups. Fasciculations were observed especially in forearm muscles and it was observed that he had been avoiding head movements because of painful muscle cramps. Deep tendon reflexes were hypoactive. Nerve conduction studies were normal. By needle electromyography, giant motor unit action potentials (amplitudes up to 8 mV), fibrillation potentials, positive sharp waves and fasciculation potentials were detected in all muscles which were investigated. A hypercellular bone marrow (100%) was determined by bone marrow biopsy. In addition to increased production of the myeloid and megakaryocytic lines, abnormal aggregation and grouping of megakaryocytes were seen. Reticular fibers were increased. He had some benefit of dyphenilhydantoin treatment given for the painful cramps in his neck and forearm muscles. Hydroxyurea treatment was started for myelofibrosis. Six months later, his general condition was better, and the painful cramps were completely resolved. No marked deterioration has been detected in neurologic examination and electromyography for 1 year.

Atrophy↗
PubMed2003

Traumatic atypical Brown-Sequard syndrome: case report and literature review.

A man was kicked on the neck, 10 days after which he noted right-sided numbness. Clinically, he had diminished deep tendon reflexes over the left upper limb, absent left superficial abdominal reflexes, a left extensor plantar response, mild left hemiparesis, diminished pinprick, temperature and vibratory sensation up to the right T(4-5) dermatome and diminished proprioceptive sensation in the right upper and lower limbs. Cervicothoracic magnetic resonance imaging (MRI) revealed a left C(6-7) posterolateral disc prolapse with indentation and oedema of the cord at the same level. He was given intravenous dexamethasone, with mild resolution of his motor but not his sensory symptoms. Transcranial magnetic stimulation and evoked potentials performed 3 days later were unremarkable. He was discharged soon after, preferring to seek traditional therapy in his country. We attempt to explain the anatomical basis for his clinical signs, review the literature for similar cases, and examine the usefulness of available treatment and investigations.

Adult↗
PubMed2003

Increased CSF protein in chloroquine-induced axonal polyneuropathy and myopathy.

OBJECTIVES: Few data are available about myopathy and polyneuropathy as rare side effects of chloroquine treatment. Even more rarely are cerebrospinal fluid (CSF) abnormalities in chloroquine polyneuropathy/myopathy. CASE DESCRIPTION: The patient is an 81-year-old woman with a 30-year history of chronic polyarthritis. As a basic therapy, she received chloroquine (250 mg per day) since 1997. Already, 1 year later she developed slowly progressive gait disturbance, which led to recurrent falls, and forced her to use crutches and other orthotic devices. Since March 2001, she was no longer able to climb stairs. Since then she also developed sensory disturbances in both lower limbs. Clinical neurological investigation revealed weakness and wasting of all four limbs and reduced tendon reflexes and stocking-type sensory disturbances. Nerve conduction studies were indicative of an axonal polyneuropathy. Electromyography was non-specifically abnormal. Muscle biopsy of the gastrocnemius muscle disclosed neuropathic and myopathic features and frequent fibers with partially rimmed vacuoles, containing concentrically or parallelly sliced inclusions. CSF investigations disclosed increased protein but otherwise normal findings. Five months after discontinuation of chloroquine and replacement by leflunomid, there was marked clinical improvement. CONCLUSIONS: Chloroquine polyneuropathy/myopathy may go along with increased CSF protein. Discontinuation of the causative agent results in prompt recovery of the described abnormalities.

Aged↗
PubMed2002

Phase I safety assessment of intrathecal ketorolac.

Spinal prostaglandin synthesis has been implicated in acute pain processes and in generation and maintenance of central sensitization, and intrathecal injection of cyclo-oxygenase (COX) inhibitors produce antinociception and reduce hypersensitivity in animals. We herein report a Phase I safety assessment of intrathecal injection of the COX inhibitor, ketorolac, in healthy volunteers, and demonstrate no serious side effects. Preclinical studies suggest a major site of action of COX inhibitors for analgesia lies in the central nervous system, especially the spinal cord. For example, COX isoenzymes are expressed in the spinal cord, acute noxious stimuli and inflammation increase spinal prostaglandin production, and spinally administered prostaglandins excite dorsal horn projection neurons, induce release of excitatory neurotransmitters, and cause nociceptive behavior. Intrathecal injection of COX inhibitors increases thermal and mechanical withdrawal threshold in animals with inflammation or nerve injury at doses several 100-fold less than those required systemically. Following pre-clinical neurotoxicity screening and regulatory agency approval, we examined the safety of intrathecal injection of a preservative-free formulation of the COX inhibitor, ketorolac. In an open label, dose-escalating design, 20 healthy volunteers received intrathecal ketorolac, 0.25, 0.5, 1, or 2mg (n=5 per group). Ketorolac did not alter blood pressure, although there was small (10-12%), dose-independent reduction in heart rate for the first hour after injection when data from all subjects were pooled. Ketorolac did not affect sensory or motor function or deep tendon reflexes, and there were no subjective sensations, neurologic or otherwise, reported by the volunteers. Ketorolac did not reduce pain report to heat stimuli applied to the lateral calf. One subject had a mild headache 24h after study, resolving the next day. There were no long-term side effects 6 months after study. These data suggest that intrathecal ketorolac does not produce a high incidence of serious adverse events, and they support further investigation for analgesia.

Adolescent↗
PubMed1986

[Electro-clinical monitoring of peripheral neuropathies in Waldenström disease treated with plasmapheresis].

The aim of this study was to determine the effects of plasma exchange (PE) associated with Chlorambucil in the treatment of peripheral neuropathies in four patients suffering from Waldenström's disease (three cases with IgM kappa paraproteinemia and one case with IgM lambda). Before PE therapy, there was a severe slowing down of the motor and sensory conduction velocities (MCV and SCV) in three cases (IgM kappa) and a less severe slowing in one case (IgM lambda). In three cases, PE rapidly (as early as the third or the fourth administration) brought about a moderate improvement in the MCV and SCV, especially in the upper limbs, whereas in one case, no effect was noted. Clinically, the paraesthesias and dysaesthesias diminished, but the deep tendon reflexes remained absent or markedly depressed. Three months after the PE, nerve conduction velocities were again very reduced. The current literature on the physiopathological mechanisms of the peripheral neuropathies in the Waldenström's disease and the effects of the treatment by immunosuppressive agents and PE are reviewed.

Electromyography↗
PubMed2000

Autosomal recessive early-onset parkinsonism with diurnal fluctuation: clinicopathologic characteristics and molecular genetic identification.

Autosomal recessive early-onset parkinsonism with diurnal fluctuation (AR-EPDF, syn. autosomal recessive juvenile parkinsonism, PARK2) is one of the hereditary parkinsonian syndromes. We examined subjects consisting of 43 patients from 22 families with AR-EPDF. The clinical features were relatively homogeneous, including the average age at onset of 26.1 years, beginning with dystonic gait disturbance, diurnal fluctuation of the symptoms (sleep benefit) unrelated to medication, dystonia (mainly foot dystonia), hyperactive tendon reflex, remarkable effect of levodopa and other antiparkinsonism drugs, susceptibility to dopa-induced dyskinesia, mild autonomic symptoms, absence of dementia, and slow progression of disease. Some patients had hysteric character or psychic symptoms provoked by medication. Pathologic study revealed neuronal loss in the substantia nigra pars compacta and locus coeruleus without Lewy body formation. We performed extensive molecular genetic analysis of the parkin gene in 16 families to identify a total of six different deletional mutations. In AR-EPDF loss of newly discovered 'Parkin' protein is responsible for selective degeneration of the pigmented neurons in the substantia nigra and locus coeruleus. Compared with autosomal dominant Parkinson's disease, AR-EPDF appears to be more prevalent and present in several ethnic groups.

Adolescent↗
PubMed2004

Clinical and neurophysiological characteristics of congenital myasthenic syndromes presenting in early infancy.

The congenital myasthenic syndromes (CMS) constitute a group of genetic disorders, which affect neuromuscular transmission, presenting usually within the first years of life and with a clinical spectrum ranging from mild muscle weakness to severe disability with life-threatening episodes. We present clinical and neurophysiological data of 11 patients (four males, seven females) with CMS diagnosed during the last 5 years. Eight of the 11 patients presented immediately after birth and the remainder by 10 months of age; eight patients had contractures at birth and seven of them required assisted ventilation either immediately in the neonatal period, or at some point afterwards due to respiratory distress or recurrent apnoeas. Neurological signs at presentation were: in nine patients profound hypotonia, in five absent tendon reflexes, in seven ptosis and in eight bulbar signs. In six patients an edrophonium test was performed: only three of them had a positive response; however, eight out of 11 patients responded at least partially at some point in their illness to pyridostigmine. Diagnosis of CMS was confirmed either by demonstration of a decrement after repetitive nerve stimulation or by increased instability and jitter after stimulated single fibre EMG. In five patients, there was a positive family history with death of at least one previous sibling with an undiagnosed neuromuscular disorder. As regards final outcome, five patients died at ages ranging from 1 to 17 months, two patients are still ventilator-dependent at 3 and 5 months of life, respectively, and four patients still survive with either a mild or a moderate motor delay (follow-up range 8-38 months). None of the clinical or neurophysiological characteristics were correlated with outcome (Fisher's exact test). We conclude that a significant number of CMS patients may present in the neonatal period with a variable clinical expression and usually with a poor prognosis. The recognition of specific clinical constellations combined with a search for aetiology at a molecular level will enable the further characterisation of subgroups of CMS.

Age of Onset↗
PubMed2004

Right thalamic hemorrhage resulting from high-voltage electrical injury: a case report.

A 12-year-old boy was admitted with electrical burn and loss of consciousness. On physical examination his general condition was poor. Extensive burn areas, second and third degree, were present on his face, scalp, bilateral auricles, right cervical region, shoulders, right axilla, upper region of the thorax, and proximal region of the upper extremities. The total burned surface area was about 25%. Pupils were isocoric, but response to light was bilateral poor. He was stuporous and responsive only to pain. Deep tendon reflexes were exaggerated and plantar responses were bilateral extensor. Bilateral decorticate rigidity was noted. Computerized tomography of brain revealed brain edema and right thalamic hemorrhage. Magnetic resonance imaging of brain, examined 25 days after admission, revealed right thalamic hemorrhage and mild right subdural effusion. He was discharged form hospital 40 days after admission. However, spastic quadriplegia and severe mental retardation remained as sequela. On the 4th month of follow-up, no improvement was noted in his neurological examination. On the 9th month of follow-up, his clinical condition was better, but bilateral electric cataract was diagnosed. Both eyes were operated on and intraocular lenses were implanted with good results. Now he is 16th month of follow-up: neurological examination revealed only mild hemiparesis on the left side and mild articulation disorder. His school performance was moderate and intelligence quotient was 71. Magnetic resonance imaging of brain showed markedly improvement of the hemorrhage. To our best knowledge thalamic hemorrhage resulting from high-voltage electrical injury has not previously been reported in the literature.

Brain Edema↗
PubMed1991

Mental retardation in congenital nonprogressive myopathy with uniform type 1 fibers.

A 12-year-old girl with proximal muscle weakness and delayed psychomotor development from early infancy is presented. She had a myopathic face, high-arched palate, nasal tone vocalization, positive Gowers' sign, waddling gait and decreased deep tendon reflexes. Her IQ was 40 (PIQ = 39, VIQ = 51). The serum creatine kinase level and peripheral nerve conduction velocity as well as electrocardiogram were normal. The electromyogram showed myopathic changes. Magnetic resonance imaging (MRI) of thigh muscles revealed fatty infiltration of all muscle groups, the hypertrophic biceps femoris and semimembranous muscles being spared. A biopsy specimen from the left biceps brachii muscle revealed small caliber fibers, increased variability of fiber size and uniformity of type 1 fibers (greater than 99%). This case was diagnosed as having congenital nonprogressive myopathy with uniform type 1 fibers, and had a non-deteriorating clinical course as in most congenital nonprogressive myopathy cases.

Child↗
PubMed1990

Peripheral nerve involvement in the Rett syndrome.

Clinical and neurophysiological studies were performed on 4 girls aged 9 to 19 years with the Rett syndrome (RS) (stages II and III). In addition to constant foot deformity (pes planus) and brisk tendon reflexes in the lower limbs, they showed muscular atrophy of the calves and mild atrophy of the extensor digitorum brevis muscle. Motor NCVs were within normal values for age, but distal latencies in two girls and compound action potential in one were abnormal, suggesting mild distal, predominantly motor neuropathy. The upper limbs showed nothing abnormal except for mild hand deformities. Neuropathology in 2 autopsy cases (aged 11 and 17 years, stage IV) and sural nerve biopsies in three girls aged 2, 3 and 17 years, all clinical stage II-III without inanition, revealed mild distal axonopathy without demyelination. Selected axons in sural nerve of a girl aged 17 and in the dental pulp of a girl aged 9, both at clinical stage II, showed increased numbers of neurofilaments. Skeletal muscle in two girls aged 11 and 17 years (both stage IV) exhibited mild alterations in the sarcoplasmic reticulum with occasional disordered myofibrils and tubular structures in the Z-filaments, but no neurogenic atrophy or abnormal mitochondria. The reported data do not support spinal denervation (motor neuron degeneration) in RS, but suggest late onset denervation due to mild distal axonopathy of hitherto unknown origin.

Adolescent↗
PubMed1991

A rare case with diurnal fluctuation of head instability, hypotonia and choreoathetotic movements improved by L-dopa treatment.

This report concerns a 6-year-old girl who showed peculiar symptoms but responded favourably to L-dopa. She developed normally until around 1 year of age, at which time head instability, hypotonia, increased deep tendon reflexes and choreoathetotic movements developed. These symptoms appeared to worsen in the afternoon and were alleviated after sleep. An extremely small dose of L-dopa (2 mg/kg) showed dramatic effects and her symptoms disappeared. This condition may be associated with the supersensitivity of the dopamine receptors, caused by hypofunction of the dopamine neurones.

Child↗
PubMed1990

Hypocalcemic hyper-CK-emia in hypoparathyroidism.

A 15-year-old boy with increased serum creatine kinase (hyper-CK-emia) due to hypocalcemia in turn caused by idiopathic hypoparathyroidism (HP) is presented. Hyper-CK-emia was incidentally noted while managing a patient, aged nine, with mental retardation, epilepsy and mild hypocalcemia. Neurological examination showed normal deep tendon reflexes and no muscle weakness; electromyogram was normal. The hyper-CK-emia normalized during treatment for the hypocalcemia. Previously reported patients with hypocalcemic hyper-CK-emia or myopathy together with HP are discussed, as well as the degree of hypocalcemia and the wide spectrum of the muscle dysfunction.

Adolescent↗
PubMed1987

Nonspecific congenital myopathy (minimal change myopathy): a case report.

A 28-month-old male with generalized hypotonia and muscle weakness, a myopathic face, skeletal dysmorphism and delayed motor milestones from birth is reported. He gradually developed the ability of sitting and rolling over, but could not stand without support until 28 months. There was no intellectual impairment or seizures. Deep tendon reflexes were absent. The serum CK value, peripheral nerve conduction velocity and EMG were within normal limits. A muscle biopsy specimen showed mild variation in fiber size, and an increased number of type 2C fibers on histochemical examination, but no apparent abnormalities on electron microscopy. The baby was tentatively diagnosed as having minimal change myopathy or nonspecific congenital myopathy which is thought to be one of the congenital nonprogressive myopathies.

Humans↗
PubMed1998

Childhood autism: the need for physical investigations.

In this paper the results of an extensive medical investigation of 25 children with childhood autism are presented and compared with those found in a group of non-autistic individuals matched for sex, age and intellectual level, all referred for developmental deviancy of unknown etiology. The examination included a psychiatric assessment and a neurological examination in addition to neurophysiological, chromosomal, metabolic and neuroimaging evaluation. In the clinical examination macrocephaly was found only among the autistic individuals, while the frequency of pathological cerebral CT and clinical parameters such as tendon reflexes and mobility problems was significantly greater in the control group. All the other pathological findings were found to occur with the same frequency in the two groups. Except for research purposes this study did not lend support to those who argue for extensive medical examinations for all children with autism. Based on the present findings, ordinary procedures for assessment of developmentally delayed children should be followed. This should include a systematic clinical neuropaediatric examination, an assessment of vision and hearing and a chromosome study, including that for fragile X.

Adolescent↗