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Query: UMLS:C0004134 (ataxia)
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Three cases of cystic neurinoma arising from the upper cervical spinal nerve roots and extending to the posterior cranial fossa through the foramen magnum were reported. Case 1 was a 52-year-old female presenting marked bilateral papilledema, hyperactive right knee jerk, left positive Gordon reflex and trunkal ataxia. The mass was mostly cystic and arose from the left 1st cervical nerve root. It extended to the posterior fossa, occupied the cerebello-medullary cistern and displaced the left cerebellar hemisphere posteriorly and superiorly. Case 2 was a 39-year-old male presenting marked bilateral papilledema, neck stiffness, dysfunction of the right 7, 9, 10 and 11th cranial nerves, gaze nystagmus, Horner's syndrome, right limb ataxia, and ataxic gait. The mass was totally cystic containing yellowish fluid and was growing from the right 2nd cervical spinal nerve root. The mass extended to the posterior cranial fossa up to the right cerebello-pontine angle and compressed the medulla oblongata, upper cervical cord and 7th through 11th cranial nerves on the right side. Case 3 was a 66-year-old male presenting marked bilateral papilledema, gaze nystagmus, left hemiparesis, bilateral hyperactive deep tendon reflexes, numbness of the left fingers and ataxic gait. CT scanning revealed in the midline of the posterior cranial fossa a low density mass which was enhanced in a ring-like fashion. Vertebral angiograms showed an avascular mass displacing the PICAs upwards and elongating its cranial loops antero-posteriorly. The mass was totally cystic, arose from the left 2nd cervical spinal nerve root, extended to the posterior cranial fossa and occupied the cisterna magna and vallecula. Foramen magnum syndrome was discussed and the symptoms and signs presented in these three cases were compared with those presented by foramen magnum meningioma in other reports.
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PMID:[Three cases of cystic neurinoma arising from the upper cervical nerve roots and extending into the posterior cranial fossa (author's transl)]. 732 70

We presented a rare care who had right frontal lobe infarction, with left side pseudoataxia, and the mechanism, causing pseudoataxia, was considered. The patient, a 51 year-old, righ-handed male, was admitted on August 9, 1980, complaining of left-side pseudoataxia. About p.m. 7:00, July 29, 1980, he suddenly noticed numbness of the left foot, and he found himself difficulty in standing in the next morning. He had a mild paresis and tactile-tactile of the left side including the face, which was rapidly improved. However, there was pseudoataxia of the left extremities, which had not been improved. On physical examination, dysarthria, aphasia, finger agnosia, difficulty in right left orientation or muscle weakness was not recognized, and there was no sensory disturbance except for slight impairment of stereognosis, two point discrimination and vibratory sense. Demonstrable impairment of tactiletactile from was observed in the left hand. Notable dysmetria, terminal tremor and dysdiadochokinesia were seen in the left limbs, which were remarkably worsened with eyes closed. However, tapping and line-drawing tests were normal. Babinski-Weil's test disclosed typical compass gait. There was marked swaying in Romberg position. Tandem gait was impossible with a tendency to decline the left. Deep reflexies were normal except for mildly hyperactive radial reflex in the left. Carotid and vertebral angiographies revealed neither evidence of vascular occlusion nor displacement of vessels CT scan demonstrated a low density area, which included the right inferior and middle frontal gyri, the head of the right caudate nucleus and a part of anterior crus of right internal capsule. There was enlargement of anterior horn of the right lateral ventricle. Caloric test, electronystagmography, eye tracking test or optokinetic nystagmus test disclosed no abnormalities. Vibration induced falling, which is the postural reaction to muscle vibration during standing (Ekuland, G., 1972), was not recognized when the left Achiles' tendon was stimulated. Pseudoataxia of this patient differed from the typical cerebellar or vestibular ataxia. From a review of the literatures concerning frontal pseudoataxia, almost all cases had no distinct cerebellar signs, and showed positive Romberg's sign. The impairment of tactile-tactile form and postural reaction to vibratory stimulation to the left leg, appeared in this case, could be hardly explained by the lesion of parietal lobe or deconnection syndrome. Sensory perception of parietal lobe and pyramidal motor system were thought to be almost normal in this case. Therefore, these findings should be due to impairment of integration center between sensory and motor systems. The pseudoataxia in frontal lesion seems to occur as the results of involvement of this center, in which caudate nucleus maybe has important role, but not as the results of disturbances in the front-ponto-cerebellar or front vestibular pathway.
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PMID:[Frontal pseudoataxia, discussion on its mechanism (author's transl)]. 732 87

A 28-year-old male was admitted to our hospital with the complaints of numbness of the left upper limb and gait disturbance. Neurological examination disclosed slight left dysmetria, truncal ataxia and sensory disturbance at the dermatome of C8 and Th1. CT and MRI scans showed a large mass lesion in the left posterior fossa, ventricular dilatation, cavum septi pellucidi and cavum Vergae, empty sella, cervical syringomyelia and left tonsilar herniation. The tumor which attached to cerebellar tentorium was totally removed and a histological diagnosis of meningothelial meningioma was made. Postoperative MRI scan demonstrated a disappearing of syringomyelia with the improved tonsillar herniation. Association of syringomyelia with brain tumor is relatively rare, so its pathogenesis was discussed.
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PMID:[Syringomyelia associated with tentorial meningioma]. 754 27

A patient with aosmia and night blindness had repeated clinical and electrophysiological examinations during a 21-year period. Within the first 11 years, he experienced two subacute episodes of numbness with weakness and ataxia. Over the 10 ensuing years, no additional functional disability appeared. We looked retrospectively for a correlation between repeated manual muscle scoring and different nerve conduction parameters. Further studies were done in order to estimate reinnervation in proximal and distal muscles and to assess autonomic functions. A direct relationship was found between the magnitude of muscle weakness and the amplitude of compound muscle action potentials, whereas nerve conduction velocities were inhomogeneously reduced but almost unchanged over time. Parasympathetic tests were normal but sympathetic skin responses were absent. As estimated by macro-EMG and turns-amplitude analysis the compensatory reinnervation was very high. We conclude that, in Refsum's disease, recurrent segmental demyelination of a significant portion of the motor units can occur in parallel with exacerbations of weakness, and that a considerable degree of progressive motor and sudoromotor axonal loss can be found although there is an apparent long-term clinical stabilization of the neuropathy.
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PMID:Quantitative EMG analysis and longitudinal nerve conduction studies in a Refsum's disease patient. 768 25

We report a 65-year-old woman with progressive multiple cranial neuropathy. She had been suffered from bronchial asthma since 1979 for which prednisolone had been prescribed. She noted an onset of pain around her nose in October, 1989, which extended into the periorbital regions bilaterally. In February, 1990, she was treated with stellate ganglion block and trigeminal nerve block; these treatments partially alleviated her pain. In May of 1991, she noted a difficulty in swallowing solid foods. In November of the same year, she developed right facial paresis; two weeks later, she noted numbness in her left face, and was hospitalized to our service on December 16, 1991. On admission, she was afebrile and general physical examination was unremarkable except for piping rales in her both lung fields. On neurologic examination, she was alert and oriented to all spheres; higher cerebral functions were intact. In the cranial nerves, her olfactory sense was lost bilaterally; her vision was markedly diminished bilaterally only to recognize hand movements; the optic fundi appeared normal; the pupils were isocoric and reacted to light promptly. The extraocular muscles were moderately weak to most of the directions more on the left; no nystagmus was present. Facial sensation was diminished bilaterally; the jaw deviated to right; right facial paresis of peripheral type was present; her hearing was diminished bilaterally more on the right. The movement of the soft palate was diminished on the right side; dysphagia was present; her voice was horse; the gag reflex was diminished. The sternocleidomastoid muscle was weak bilaterally; the tongue appeared normal. Examination of gait was differed because of headache, however, no apparent motor weakness was present. No ataxia or involuntary movement was noted. Deep reflexes were normally elicited and symmetric. Plantar response was flexor. Sensation in the extremities was intact. Kernig's sign was positive at 70 degree leg extension; eyeball tenderness was also present bilaterally, however, no nuchal stiffness was noted. Following abnormalities were present in the laboratory examination: WBC 11,400/microliters, ESR 50 mm/hr, CRP 6.1 mg/dl. The lumbar CSF was under a normal pressure containing 29 WBC/microliters (neutrophils 7, lymphocytes 20, others 2), 67 mg/dl of protein, and 53 mg/dl of sugar; cultures for acid-fast bacilli as well as for other bacteria were negative; no malignant cells were found. A cranial CT scan revealed an isodensity mass in the orbit and ill-defined low density areas in the white matters of the frontal lobes.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 65-year-old woman with headache, facial pain, and progressive multiple cranial neuropathy]. 787 85

As dizziness can be caused by so many different pathophysiological mechanisms, it is crucial to determine the type of dizziness before proceeding with the diagnostic evaluation. Vertigo, defined as an illusion of movement, is an important subtype of dizziness that indicates a lesion somewhere within the vestibular system. Probably the most useful feature for differentiating between peripheral and central causes of vertigo is the associated symptoms. Vertigo of peripheral origin is typically associated with auditory symptoms such as hearing loss and tinnitus, while vertigo of central origin is nearly always associated with neurological symptoms such as diplopia, weakness, numbness and ataxia. Each of the common causes of vertigo has a characteristic clinical profile that should suggest a likely diagnosis after the history and examination are complete. Probably the most important treatment breakthrough is the positional manoeuvre that reliably cures benign positional vertigo (see Chapter 6). The treatment strategy for an acute peripheral vestibular lesion has evolved over the past few years. Patients are encouraged to return to normal physical activity as rapidly as possible. Repeated head, eye and body movements (vestibular rehabilitation) help the brain to recalibrate the relationship between visual, proprioceptive and vestibular signals (Chapter 9).
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PMID:Approach to the dizzy patient. 787 2

Presently, the course of multiple sclerosis (MS) can be altered little, if at all. Appropriate symptom management, however, can change the course of lives and allow for more comfortable, healthier living despite significant disease. Symptoms in MS are divided into three broad categories. Those that result from actual demyelination include decreased vision, weakness, spasticity, bladder problems, ataxia, numbness, and decreased cognition. Secondary symptoms spring from the primary; these symptoms include contractures, urinary tract infections, megacolon, decubiti, decreased bony calcification, and muscle atrophy. Tertiary symptoms are the unavoidable psychological, vocational, and social problems that occur with chronic disease. This article reviews standard therapies, but the emphasis is on newer management solutions that may not have reached their full potential, though they add to the development of an appropriate life-management plan for persons with MS. The pharmacological approach to symptom management is emphasized, while understanding that rehabilitation and medications cannot be separated in the real life alleviation of MS symptoms.
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PMID:Symptom management in multiple sclerosis. 801 73

A 58-year old right-handed man with chronic non valvular atrial fibrillation developed an acute left upper limb ataxia with transient numbness and mild motor impairement. Two weeks later, there was a severe degree of ataxia of the left upper limb and prominent asterixis of the left hand. CT scan and MRI showed a small parietal infarct. Initial median nerve somatosensory evoked potentials (SEPs) showed mild impairement of right parietal responses with absent right frontal SEPs P22 and N30. Two months later, parietal responses were normal but right frontal SEPs P22 and N30 remained abolished while ataxia of left upper limb persisted. Electromyographic activity recorded at the same time showed periodic involvement of the left hand distal tonus. These finding suggested that both ataxia and asterixis were due to a single postcentral infarct. Frontal SEP components are known to convey proprioceptive inputs which could be received by neocerebellar afferent pathways. Generators of these components are presumably located in premotor cortex and can be activated through parietofrontal connections. In our case it can be assumed that the parietal infarct involved these connections, which are mainly implied in the regulation of postural tonus of the distal upper limbs, and simultaneously impaired neocerebellar afferent pathways resulting in the emergence of parietal ataxia.
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PMID:[Ataxic monoparesis of the upper limb and suspension of the tonus caused by parietal lesion]. 823 23

A 67-year-old woman experienced a severe headache and vomiting. A computed tomographic (CT) scan showed a mild subarachnoid hemorrhage. Cerebral angiography revealed a saccular aneurysm at the apex of the basilar artery. Several days later, she noticed mild hemiparesis of the left extremities. She underwent a clipping operation on the aneurysm by approaching from the right temporal love. Postoperatively, she developed diplopia and dilatation of the left pupil. Cerebral angiography revealed an occlusion of the left posterior cerebral artery. She was admitted to another hospital in order to continue rehabilitation. General physical examination was normal. Neurological examination revealed paralysis of the left medial and left inferior rectus muscles and palsy of the left inferior oblique muscle. The pupil of the left eye was dilated, measuring 5 mm in diameter, and it did not constrict to any stimuli. The left superior rectus and levator palpebrae superioris functioned normally. Visual acuity and visual fields were normal except for the influence of a senile cataract. She had a mild left hemiparesis, slight left ataxia and slurred speech. She had numbness of the left half of the body. A CT scan showed small low density areas in the right thalamus and left cerebellar hemisphere. Her ophthalmologic findings were compatible with the inferior branch palsy of the oculomotor nerve. The ophthalmoplegia of this case seems to be due to partial damage of the oculomotor nerve induced by ischemia of vascular supply. It is supposed to be caused by a vasospasm of the left posterior cerebral artery following a clipping operation of the basilar apex aneurysm.
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PMID:[Inferior branch palsy of the oculomotor nerve following clipping of basilar apex aneurysm]. 831 94

We report a 57-year-old man who developed Wallenberg syndrome and vertebral artery dissection, probably as a complication of neck rotation during golf exercise. He noticed pain in the neck during golf exercise. About 16 hours later, he developed numbness in the right hand, cold sweat, vertigo, hiccup, double vision and ataxia in gait. Neurological examination on the 22nd day revealed a right Wallenberg syndrome. The right vertebral angiogram showed a marked stenosis of the vertebral artery at the portion across the dura, and a dissecting aneurysm in the portion from its entrance into the posterior fossa through the exit of the right posterior inferior cerebellar artery. Quick rotation and/or extension of the neck and head during golf exercise probably caused the vertebral artery dissection, resulting in Wallenberg syndrome. More attention should be paid to relatively trivial trauma as the cause of stroke, especially in the victims of younger ages.
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PMID:[Wallenberg syndrome and vertebral artery dissection probably due to trivial trauma during golf exercise]. 833 99


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