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PubMedDate not supplied

Blepharospasm and apraxia of eyelid opening in lithium intoxication.

We present the case of a 72-year-old woman with a history of a bipolar mood disorder chronically treated with lithium. Upon having the dose increased, she developed an acute confusional state accompanied by blepharospasm (BS) and apraxia of eyelid opening. Gait instability with frequent falls, pyramid tract signs, and postural tremor in both hands were also evident. On withdrawing lithium, symptoms remitted within 2 weeks. This patient illustrates that BS and apraxia of eyelid opening may be triggered by lithium overdose. Our case warrants the inclusion of lithium in the list of drugs liable to induce such movement disorders.

Aged↗
PubMed1999

Vitamins and brain development.

Effects of deficiency of vitamins on early development of brain have been reviewed. Unusual developmental problems in neurogenesis specific for the brain and impairment of its functional capacities due to vitamin deficiency have been discussed. The species-specific "critical periods" in development of various systems have been mentioned. Indices such as reflex activity, locomotion, special senses, cognition and adaptive behavior were used for assessing brain maturation in experimental models and humans. Significant examples include brain anomalies in humans and other mammals caused by retinoid excess or deficit; increase in calbindin D28K, a vitamin D dependent calcium-binding protein during postnatal period in rat; hydrocephalus and exencephaly in prenatal rats and subarachnoidal or intracerebral hemorrhage in infants caused by vitamin E deficiency. Peripheral neuropathic lesions leading to infantile beriberi is caused by thiamine deficiency. Impaired growth in retinal layers leading to delay in maturation of electroretinogram and depth-perception in postnatal rats occur due to pyridoxine deficiency. Infants of severely vitamin B12 deficient mothers show abnormalities in behavior involving basal ganglia and pyramidal tract. Folic acid deficiency results in delayed maturation of the basic electroencepalographic patterns. In addition, vitamin-interactions leading to developmental errors have been pointed out. Vitamin B6 deficiency impairs vitamin B12 absorption and biotin deficiency may be aggravated by pantothenic acid deficiency. Vitamin C deficiency resulting in impaired metabolism may produce symptoms of deficiency of folic acid. Another characteristic examples is that iron absorption from dietary sources is dependent on ascorbic acid.

Animals↗
PubMed1999

[An autopsy case of motoneuron disease with dementia of long duration].

An autopsy case of MND with dementia, 67 years old, man, was reported. The behavioral disturbance appeared at 61 years old, and was followed by the upper limb weakness and respiratory failure. He had remained on a respirator for 56 months. The total duration of the disease was 74 months, which was far longer than mean duration of the cases previously reported, 25-30 months. The pathological findings were about essentially identical to those mentioned before, such as cortical alterations in temporal and frontal lobes, neuronal loss with gliosis in amygdaloid body and substantia nigra, and loss of lower motoneurons in anterior horn of spinal cord and in the several motor cranial nerve nuclei. There were several Bunina bodies in the remnant lower motoneurons, but no changes in the pyramidal tracts or loss of Betz cells in the precentral gyrus. Intracytoplasmic ubiquitin-immunopositive inclusions in the granule cells of hippocampal dentate gyrus were also encountered, but the number of which did not increased, compared to the preceding data. There may be frequently little correlation between the disease duration and the number of such inclusions. The regional alteration in the intermediate zone between subiculum and entorhinal cortex was revealed also at the level of the splenium of corpus callosum. It has been reported that such parahippocampal lesion may initiate at the anterior part of temporal lobe and become undiscernible at more posterior level than the lateral geniculate body. The formation of such parahippocampal lesion may be concerning with the length of disease duration. In addition, there were numerous senile plaques, diffuse or neuritic type only in the parietal lobe cortex without any other changes.

Aged↗
PubMed1999

[A case of Bickerstaff's brainstem encephalitis which started with Wallenberg's syndrome].

A 54-year-old female developed dysarthria, left limb ataxia, and crossed dissociated sensory impairment, followed by external ophthalmoplegia, severe bulbar palsy and bilateral pyramidal tract involvement. A high titer of anti-GQ1b IgG antibody was detected in her serum. Brain MRI (T2 weighted image, diffusion weighted image) and peripheral nerve conduction study were normal. We diagnosed her as having Bickerstaff's brainstem encephalitis. In the past literature, we could not find any case of Bickerstaff's brainstem encephalitis showing crossed dissociated sensory impairment.

Autoantibodies↗
PubMed2000

[Transient improvement in motor function and hemineglect by vestibular stimulation in a patient with right middle cerebral artery embolism].

A 62-year-old Japanese man presented left hemiparesis and left visuospatial hemineglect following a right hemispheric stroke. His CTs and MRIs of the brain revealed a large embolic infarction of the middle cerebral artery territory. A month after the cerebrovascular event, his weakness of the left lower limb almost recovered fully. However, his upper limb motor function was still disabled; in particular, his ability of finger flexion in the left hand was almost lost. Then, vestibular stimulation using either a cold caloric stimulation to the left ear or a warm caloric stimulation to the right ear was performed, and the effect on the hemineglect symptoms were assessed by a line bisection task. After vestibular stimulation, not only his hemineglect symptoms but also his motor functions of left upper limb transiently improved; he became able to make a fist. The improvement of his hemineglect symptoms was obtained by vestibular stimulation using either a cold or a warm caloric stimulation. However, the effect on the motor function was obtained only by the cold caloric stimulation applied to the left ear. Based on the effect of the vestibular stimulation, we postulates that the impairment of the motor function in the present patient is not only a paresis caused by the pyramidal tract lesion but also symptoms related to the hemineglect syndrome.

Hemiplegia↗
PubMed1999

[An autopsy case of amyotrophic lateral sclerosis/parkinsonism-dementia complex with family history and living history in the Kii Peninsula focus].

The patient was 68 year-old woman with an 8-year history of parkinsonism which was followed by psychiatric symptoms and neurogenic amyotrophy 5 years after the onset. She had a family history of parkinsonism associated with dementia in all of her three siblings. They grew up in Hobara village, a focus of amyotrophic lateral sclerosis (ALS) in the Kii Peninsula of Japan, in their childhood. Their parents were neither consanguineous nor natives of the Kii Peninsula. The brain weight was 1,040 g, and there were mild frontal lobe atrophy, moderate atrophy of pes hippocampi, decoloration of the substantia nigra and locus ceruleus, and anterior spinal root atrophy. The microscopic examinations revealed degeneration of CA 1 portion of the hippocampus to parahippocampal gyrus, substantia nigra, locus ceruleus and spinal anterior horn with Bunina body. The spinal pyramidal tracts also degenerated mildly. The neurofibrillary tangles (NFT) were observed in the cerebral cortex, especially in the cortices through hippocampus to lateral occipitotemporal gyri, basal nucleus of Meynert, basal ganglia, thalamus, substantia nigra and widespread regions of the central nervous system through the brainstem to the spinal cord including the nucleus of Onufrowicz. In spite of a few amount of the senile plaques in the cerebral cortex and Lewy bodies in the substantia nigra and locus ceruleus, abundant NFT distributed mainly in the third layer of the cerebral cortex, which is the characteristic finding of amyotrophic lateral sclerosis/Parkinsonism-dementia Complex (ALS/PDC) in the island of Guam. Thus this was verified ALS/PDC case outside the Guam island. The high incidence of neurological disease in her siblings and their history of living in the focus region in childhood suggest the genetic factor of ALS/PDC which is sensitive to certain environmental agents in the early stage of the life.

Aged↗
PubMed1999

Dengue infection with central nervous system manifestations.

A prospective observational study was conducted over a seven years period to determine the clinical and laboratory findings of dengue patients with central nervous system manifestations. Thirty serologically confirmed dengue infected patients with central nervous system manifestations were seen at the Department of Pediatrics, Faculty of Medicine, Chulalongkorn University, Bangkok and at Songkhla Hospital, Songkhla, Thailand. The age ranged between 3 months and 14 years with a mean age of 6.2 years. Seventeen were boys and thirteen were girls. The central nervous system manifestations included alteration of consciousness 76.7%, seizures 63.3%, pyramidal tract signs 36.7%, meningeal signs 30% and headache 26.7%. Eleven patients had primary while 19 had secondary dengue infection. Cerebrospinal fluid examination showed lymphocytic pleocytosis in 6 out of 28 patients while presence of anti-dengue IgM antibodies was detected in 2 out of 19 specimens of cerebrospinal fluid tested. Two patients died, autopsy was done on one patient and examination of the brain was compatible with viral encephalitis.

Adolescent↗
PubMed2000

[What's new in primary lateral sclerosis?].

Primary lateral sclerosis as a nosological entity distinct from amyotrophic lateral sclerosis has been the subject of controversy since it was first described in the nineteenth century. Primary lateral sclerosis has been defined as a rare, non-hereditary disease characterized by highly progressive spinobulbar spasticity, related to the exclusive loss of precentral pyramidal neurons, with secondary pyramidal tract degeneration and preservation of anterior horn motor neurons. We carried out a study in nine patients with a diagnosis of primary lateral sclerosis. Our clinical, electrophysiological and pathological investigations provide evidence that the disease has a heterogeneous clinical presentation and that degeneration is not restricted to the central motor system but also affects the lower motor neuron. In view of this similarity with amyotrophic lateral sclerosis, primary lateral sclerosis may represent a slowly progressive syndrome closely related to motor neuron disease and amyotrophic lateral sclerosis.

Adult↗
PubMed2000

X-linked congenital ataxia: a clinical and genetic study.

We report on a family in which two males are affected with X-linked congenital ataxia (XCA). Clinical manifestations include severe hypotonia at birth, delay of early motor development, slow eye movements, and nonprogressive cerebellar ataxia. The neurological examination excluded a neuromuscular disease, mental retardation, and pyramidal tract involvement. Neuroimaging showed global cerebellar atrophy in both patients that was not evident in the first years of life. The clinical findings in this family are very similar to those in a Russian pedigree [Illarioskin et al., 1996: Ann Neurol 40:75-83] and outline a recognizable phenotype. Linkage studies in our family, using 28 highly polymorphic Généthon microsatellite markers evenly distributed along the X chromosome, excluded a 24 cM interval between DXS990 and DXS424 located within the previous candidate region of 54 cM, reducing the critical interval.

Adult↗
PubMed2000

[A case with symptomatic epilepsy and mirror movement due to unilateral schizencephaly].

Schizencephaly is an extremely rare congenital disease caused by abnormal neuronal migration. The etiology of schizencephaly is not established but vascular disturbance in early childhood could cause this condition. We have cared of a patient with schizencephaly. The patient was 47 year old male. He had focal motor seizure with secondary generalization. Neurological examination revealed, mild left hemiparesis, left pyramidal signs with no sensory impairment, left hemiatrophy, and mirror movement. MRI findings showed schizencephaly, open lip type(type II) in right cerebral hemisphere. His epileptic seizure was controlled by administration of sodium valproate. The possible mechanism of this mirror movement in his left hand and leg could be reorganization of non-affected brain and disinhibition on homolateral pyramidal tract in non-affected left cerebral hemisphere by the transcallosal inhibitory pathyway from affected right cerebral hemisphere. Sodium valpronate can not suppress this mirror movement.

Anticonvulsants↗
PubMed2000

[Physiopathological and chemopathological mechanisms of central motor disorders in amyotrophic lateral sclerosis].

A complex study of pathophysiological characteristics of corticospinal systems was performed in patients with amyotrophic sclerosis (ALS) by transcranial magnetic resonance stimulation (TMRS) and estimation of the levels of mediatory amino acids in the cerebrospinal fluid (CSF). There was a time course of changes in the excitability of cortical motor neurons (MNs) and in the functional status of the pyramidal tract as ALS progressed. The large cortical MNs were found to be afflicted just at early stages by further involving their axonal systems into the pathological process. As a result, mainly fine slowly conducting axons of MNs functioned at the later stages of the disease. Neurochemical changes correlated with the duration of the disease and were supposed to play an important role in the pathogenesis of ALS. Besides, a significant correlation revealed by TMRS between the pathology of the corticospinal tract and the cerebrospinal fluid levels of glutamate confirmed the role of glutamate as a the main neurotransmitter of this motor system. The results of the study also confirm the significance of excitotoxic mechanisms in central motor disorders in ALS.

Adult↗
PubMed2000

[A family with DRPLA and chronic renal failure].

We reported a family with dentato-rubro-pallido-luysian atrophy (DRPLA) and chronic renal failure. The proband was a 66-year-old woman who developed gait disturbance, limb ataxia, pyramidal tract signs, and dementia since age 54. T2-weighted brain MR images revealed symmetric high-signal lesions in the cerebral white matter, in addition to cerebellar, brainstem, and cerebral cortical atrophy. She suffered from renal failure and became dialysis-dependent at the age of 59, four years after the onset of chronic nephritic syndrome. At the age of 66, she was admitted to our hospital because of hyperthermia and disturbance of consciousness, and died of DIC. Her CAG repeats in the DRPLA gene were 58 and 12. An autopsy was performed. The brain weighed 910 g. Histological findings confirmed the diagnosis of DRPLA. Her mother died of chronic renal failure. All three siblings had cerebellar ataxia, and two siblings had chronic nephritic syndrome. Among them, only her younger brother was diagnosed as non-IgA glomerulonephritis based on kidney biopsy findings at the age of 48. Though the nature of the association between DRPLA and renal dysfunction remains obscure, the DRPLA gene abnormality may be correlated with chronic renal failure in this family.

Aged↗
PubMed2000

[Encephalomyelopathy demonstrated on MRI in a case of chronic toluene intoxication].

Myelopathy in chronic toluene intoxication is rare. We present obvious lesions of the spinal cord on MRI in a 30-year-old Japanese man with chronic toluene intoxication. He had abused toluene for more than 10 years, and developed visual impairment, horizontal nystagmus, pyramidal tract signs, postural tremor, Romberg's sign, and sensory disturbance below the level of Th 2 dermatome. Anti-HTLV-1 antibody titer and vitamin B12 level in the serum were within normal limits. Biochemical analysis showed no increase of very long chain fatty acids. Cerebrospinal fluid showed no abnormal findings. Auditory brainstem response showed delay of I-V interpeak latency. Somatosensory evoked potential with the median nerve stimulation showed delay of N13-N20 central conduction time, which was later followed by absence of N14-N20 components. On MRI in T2 weighted image, marked high intensity was demonstrated in the posterior limbs of the internal capsule, and in the posterior columns and lateral tracts from the cervical through the upper thoracic cord. Cerebral lesions probably reflect demyelination and axonal degeneration produced by chronic toluene abuse. Spinal cord lesions seem to be secondary to nerve fiber changes more proximal to the nerve cell bodies.

Adult↗
PubMed2000

[A case of NARP (neurogenic muscle weakness, ataxia, and retinitis pigmentosa) with a T-to-C point mutation at nt 8993 of mitochondrial DNA].

We report a case of NARP with a T-to-C point mutation at nt 8993 of mitochondrial DNA. A 37-year old man with mild mental retardation, retinitis pigmentosa, and clonic-tonic seizure was admitted to our hospital. The neurological examination revealed scanning speech, dystonic neck turning to the left side, and pyramidal tract signs. Serum-, CSF-lactate and pyruvate level were slightly elevated. Brain MRI findings showed cerebral atrophy, cerebellar cortical atrophy accompanied with dilation of forth ventricle, and high intensity lesions in the bilateral lenticular nuclei on T2 weighted images. Nucleotide sequence analysis of the mitochondrial DNA in the leukocytes demonstrated a T-to-C point mutation at nt 8993. To our knowledge, this is the first report of a Japanese patient with NARP associated with the T-to-C mutation at nt 8993 of mt DNA. Mitochondrial DNA analysis should be considered in the differential diagnosis of patients with retinitis pigmentosa and various neurological signs.

Adult↗
PubMed2000

[Sudden bilateral hearing loss with vertigo due to vertebral artery occlusion].

We report a case of sudden bilateral hearing loss associated with an occlusion of the right vertebral artery. A 66-year-old man was admitted to hospital suffering from sudden onset vertigo, deafness, and vomiting. He could not walk due to truncal ataxia. There was positional nystagmus to the right; spontaneous and gaze-evoked nystagmus were absent. He had no facial nerve palsy, dysarthria, pyramidal tract signs, limb ataxia, and sensory impairment. Pure tone audiometry demonstrated a profound sensorineural deafness of both ears. A tentative diagnosis of sudden deafness was made. He was treated with intravenous infusion of corticosteroid; hearing loss of the left ear slightly improved. Cranial MR imaging demonstrated fresh small infarcts in the right cerebellar tonsil, the left cerebellar medulla, and the left middle cerebellar peduncle. MR angiography demonstrated an occlusion of the right vertebral artery. It is possible that reduced perfusion of the anterior inferior cerebellar arteries and internal auditory arteries on both sides resulted in multiple "border zone" infarcts and damage to the inner ear. Clinicians should be aware of the possibility of vertebrobasilar occlusive disease in case of sudden bilateral hearing impairment, even when brainstem or cerebellar signs are absent.

Aged↗
PubMed2001

[Subacute combined degeneration of the spinal cord: easy diagnosis, effective treatment].

Four patients, three women aged 49, 47 and 74 years, and a man aged 64 years, presented with progressive sensory deficit, pyramidal tract symptoms and postural instability. Tests revealed megaloblastic anaemia and low vitamin B12 levels. Two of the female patients had undergone gynaecological surgery with nitrous oxide anaesthesia, and the male patient had undergone a gastric resection. Subacute combined degeneration of the spinal cord is a neurological disease based on vitamin B12 deficiency. It involves the posterior and lateral columns of the spinal cord, and sometimes the peripheral nerves, the optic nerve or the brain. An MRI scan of the cervical cord revealed abnormalities for three of the four patients. Following parenteral supplementation of vitamin B12, the symptoms and the MRI abnormalities either disappeared or significantly improved. Vitamin B12 deficiency can cause subacute combined degeneration of the cord by interfering with myelin synthesis. As vitamin B12 deficiency is caused by malabsorption in the gastrointestinal tract, oral supplementation is insufficient. It is essential to recognise this treatable disease at an early stage, and not to reject the possible diagnosis if the MRI findings are abnormal. Simple blood tests can lead to the diagnosis and to effective treatment.

Aged↗
PubMed2001

[Anterior spinal artery syndrome: an important differential diagnosis of acute non-traumatic transverse spinal cord syndrome].

We report on a 77-year-old man who was suffering from pain in the chest, which was initially circumferential, along with paresthesia in his left leg, a fluctuating spastic paraparesis and dissociated sensory disturbances caudal to segment T8. In his history, he had received an aortoiliac Y-prothesis for a ruptured retroperitoneal intrarenal aortic aneurysm 39 months previously. Diagnostically, magnetic resonance imaging of the spine revealed advanced degenerative changes with osseous stenoses in segments C5-6 and less pronounced on C6-7. There were no signs of myelopathy. The results of the computerized tomogram of the neurocranium were consistent with the patient's age. The computerized tomogram of the chest and abdomen revealed a left outward bulge in the descending branch of the thoracic artery that was almost 20 mm in length. Based on the differential diagnosis, this was interpreted as an aneurysmatic sacculation with wall thrombosis or a locally circumscribed intramural hematoma upon dissection. Electrophysiologic testing by conduction of magnet-evoked potentials showed no lesions of the pyramidal tract to the extremities above the lumbosacral level. Lumbosacral stimulation evoked potentials on both sides whereas cortical stimulation did not. Based on the patient's history, the clinical findings and additional tests, the diagnosis of anterior spinal artery syndrome was rendered although its cause could not be determined with certainty. The previous transitory ischemic attack and the varying course of the disease is very exceptional in the presented case.

Aged↗
PubMed1975

Painful ophthalmoplegia: report of a case with cerebral involvement and psychiatric complications.

The diagnosis of Tolosa-Hunt syndrome should be suspected in the presence of recurrent "painful ophthalmoplegia." The most useful tests are the rapid (within 48 hours) response to steroids and positive findings on orbital venography. It should be emphasized that Tolosa-Hunt's syndrome may not be a "pure syndrome." Perhaps it is only an occasional presentation of another rather poorly understood syndrome, that of "recurrent cranial neuropathies." The present patient had at least three episodes of painful ophthalmoplegia prior to this hospitalization. During the last hospitalization, he presented with painful ophthalmoplegia, showed a rapid response to steroids, had narrowing of the carotid artery on arteriogram and an abnormal orbital venogram. However, during his hospitalization he developed involvement of cranial nerves II, III, V, VI and VII, papilledema, pyramidal tract signs and severe psychiatric disturbances, all of which remitted. This, coupled with the abnormal pneumoencephalogram and electroencephalogram and organicity on psychological testing, suggests cerebral involvement in our case.

Adult↗