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Five cases are reported of tuberculous patients who presented with hemiplegia as the initial symptom of their illness. In three patients the paralysis improved rapidly and completely with institution of antituberculous treatment. One case which came to necropsy revealed that the cause of the hemiplegia was a tuberculoma situated in the internal capsule.
The work here exposed is divided in two studies: clinical and therapeutical. 1--Clinical. The occurrence of shoulder hand syndrome has been studied in 130 patients with hemiplegia. Although the preventive treatment was correct in all cases, 90 of them developed neurodystrophy. It is shown that the appearance and the intensity of this syndrome can be predicted with some certainly as soon as three weeks after the onset of hemiplegia, since there is a statistically significant correlation with the aetiology and the existence of some associated factors. 2--Therapeutical. The efficacy of eight treatments (calcitonin, blocking agents, intravenous clomipramine, blocking agents, periarterial injections of local anaesthetics, local or general corticotherapy, physiotherapy, kinesitherapy), randomly given to the patients, was compared (90 patients and 130 treatments). Local corticotherapy was the most efficient treatment. Physiotherapy was less efficient but always well tolerated. All the other treatments were much less active. Kinesitherapy was however always necessary to prevent joint ankylosis. No correlation was found between the intensity of the shoulder hand syndrome and the efficacy of treatments.
A quadriplegic patient with a C6 lesion had a stroke with aphasia and right hemiplegia 20 years after his cervical cord injury. The combination of hemiplegia and quadriplegia created unusual rehabilitation problems, the most disabling of which was a painful flexion contracture of the right elbow that prevented any useful right arm function. A sequence of phenol nerve blocks produced almost complete resolution of this contracture and was a key factor in his successful return to independent living. Although phenol block is much less commonly performed in the upper than lower extremities, its judicious use in carefully selected cases may be beneficial to the patient's functional outcome.
Although the therapeutic effect of spinal cord stimulation (SCS) for spastic movement disorders is still controversial, its effect for multiple sclerosis has been supported by several authors. Among various clinical beneficial effects, reduction of the spasticity may be attractive for physical therapy of post-apoplectic patients. Two patients suffered from post-apoplectic spastic hemiplegia were selected for SCS. Electrodes of Medtronic's SCS system were placed at lower cervical or upper thoracic spinal cord extradura. Stimulation of 30-75 Hz in frequency and 0.3-0.5 in voltage continued for 12-14 hours during daytime every days. U.S., a 74-year-old man, suffered from cerebral infarction in the right internal capsule was treated by SCS at one year after the stroke . At the fourth day after SCS spasticity of the lower extremity reduced and his gait improved remarkably. Upper extremity also showed reduction of spasticity at the seventh day after SCS. H/M ratio before SCS was 0.85 and reduced to 0.77 at 68 th day after SCS. Recovery curve of H-wave also improved after SCS. Y.K., a 47-year-old man, suffered from pontine hemorrhage showed right spastic hemiplegia. He was treated by SCS at 13th month after the hemorrhage. Spasticity of the upper extremity reduced slightly and his gait improved obviously. H/M ratio which was 1.05 before SCS, reduced to 0.75 at 122 nd day after SCS. Recovery curve of H-wave improved remarkably after the treatment. It was obvious that the spasticity reduced after SCS and function of the extremities recovered to some extent in above patients.(ABSTRACT TRUNCATED AT 250 WORDS)
A three year old Thoroughbred filly was examined because of bilateral nasal discharge and external swelling of the left laryngeal area. Endoscopy revealed an enlarged left arytenoid cartilage, left laryngeal hemiplegia and drainage of purulent material into the lumen of the larynx. Radiographs showed a large fluid and gas filled cavity overlying the caudal larynx and cranial trachea. Surgical drainage and debridement of the abscess led to complete healing by secondary intention. Laryngeal ventriculectomy was performed as a treatment for left laryngeal hemiplegia, but a grave prognosis for respiratory soundness was given due to the extensive laryngeal fibrosis. The etiology of the Staphylococcus aureus abscess is unknown but may have originated from oral trauma to the larynx.
Of the patients with hemiplegia who had undergone active rehabilitation at the Institute of Rehabilitation Medicine (IRM), New York University Medical Center, from the years 1968 through 1977, 843 were reviewed for functional ambulatory status on admission and at discharge, type of orthotic devices used, time elapsed from onset to admission for rehabilitation, and length of stay at IRM, to determine whether a consistent change had occurred in prescribing lower extremity orthoses for patients with hemiplegia, and if so, to assess the impact of such changes on the ambulation status. Of the 843 patients reviewed, 773 (91%) were partial or nonambulators on admission. Of these, 62% of the nonambulators and 66% of the partial ambulators improved significantly. A consistent decline in the use of metal orthoses, especially of long-leg orthoses, together with an increase in the use of plastic-knee ankle-foot orthoses was demonstrated. A 20% decline in prescription of lower extremity orthoses of all kinds was also observed. The rate of neuromuscular return as mwasured by attainment of functional gait has remained stable, and the proportion of numbers of patients attaining functional gait also was unchanged.
A patient who received treatment for acute myelogenous leukemia (chemotherapy, irradiation, corticosteroid therapy) developed cerebral radionecrosis with hemiplegia (treated by corticosteroids) then multiple foci of osteonecrosis on the nonparalyzed side. The mechanisms which may have prevented osteonecrosis from occurring on the side of the hemiplegia are discussed.
From 1982 to 1991, there were 57 patients diagnosed with various intracranial disorders manifested initially with acute hemiplegia at the Department of Pediatrics, National Taiwan University Hospital. There were 33 boys and 24 girls, aged 12 days to 18 years old. In etiological consideration, cerebrovascular disease (66.7%), intracranial tumors (12.3%) and head trauma (10.5%) accounted for most of the cases. Besides acute hemiplegia, cranial nerve palsy (47.4%), disturbed consciousness (42.1%), headache (42.1%), vomiting (31.6%), focal seizure (21.1%) and fever (21.1%) were also common manifestations. Neuroimage studies of CT/MRI scan and angiography were the most useful diagnostic tools. Treatment modalities included medical treatment in 25 patients and surgical intervention in 16 patients and supportive treatment in the others. There were 12 fatal cases, half of whom died directly of intracranial pathology. The survivors exhibited various neurological deficits, in which motor deficits, mental retardation, and subsequent seizures were the three most common sequelae.
When cerebral infarction determines hemiplegia or hemiparesia which accompany a hemilateral sensitive deficit and hemianopsia and even neuropsychologic symptoms (aphasic alterations in the case of injury to the left hemisphere, heminegligence and anosognosy in the case of injury to the right hemisphere) the involvement of a sylvian artery syndrome is usually considered. Nonetheless, recent contributions have reported that such symptoms may appear in infarctions of the territory of the posterior cerebral artery. Two clinical-radiologic observations in this line are presented. Nuclear magnetic resonance demonstrated injury to the posterior arm of the internal capsule in one case and in the other the lesion developed over three times, in the latter of which injury to the cerebral peduncle was produced causing hemiparesia. The authors emphasize that hemiplegia or hemiparesia in some infarctions of the posterior cerebral artery may be due to 1) mesencephalic infarction in the posterior plane of the retromamillar Foix and Hillemand pediculum (or G. Lazorthes interpedunculum), 2) infarction or "ischemic penumbra" in the internal capsule by involvement of any of the perforating branches of the posterior cerebrum irrigating the thalamus, except for the medial posterior choroid artery or even of the Foix and Hillemand thalamus-tuberian pediculum (or Lazorthes inferior and anterior) which principally initiates at the posterior communicating branch with a fragment of the posterior branch of the internal capsule perhaps not always being under its control. In this case, the thrombus occupying the posterior cerebrum may extend to the cited communicating branch or a hemodynamic deficit may be produced in the territory of the same.(ABSTRACT TRUNCATED AT 250 WORDS)
During the third quarter of her pregnancy, a young woman with Sturge-Weber angiomatosis had a severe right hemiplegia with hemianopia and aphasia, followed 48 hours later by focal seizures. Neuroimaging did not show any cerebral lesion but contrast magnetic resonance imaging revealed a left hemispheric pial angiomatosis. The patient recovered progressively from the third day after a ceasarean. The hemianopia disappeared within 15 days, the hemiplegia within one month and the aphasia greatly improved within 3 months. Ten weeks after the clinical onset, we performed a positron emission tomography study. A decrease from 15 to 40% of the cerebral radioactivity was observed after injection of water (H2(15)O) or fluorodesoxyglucose (18FDG) in the left temporooccipital area adjacent to the meningeal angiomatosis. A chronic and focal olighemia, already reported in Sturge-Weber angiomatosis, might participate in the occurrence of this cortical metabolic depression.
Acute alternating hemiplegia in childhood is a rare disorder characterized by onset before 18 months of age and frequent attacks of alternating paralysis. In this case report, a 20-month-old boy having the diagnosis of acute alternating hemiplegia is presented. The diagnosis was based on clinical features. The frequency and severity of the hemiplegic attacks decreased following flunarizine therapy. In this case, cerebral perfusion was investigated during ictal and interictal periods. Tc-99m HMPAO-Brain single photon emission computed tomography (SPECT) revealed normal cerebral perfusion in ictal periods and hypoperfusion in interictal periods.
We report a 36-year-old woman with right hemiplegia, anosognosia, and rapidly deteriorating course. She was well until the end of January, 1995 when she had an onset of fever, sputum, and cough. A 5 x 5 tumor was found in her left lower lobe. She was admitted to the Pulmonary Medicine on May 24, 1995 when she was 36-year-old. General physical examination was unremarkable. Bone scintigraphy revealed increased uptake in the skull, sternum, right scapula, vertebrae, right femur, and in ribs. Cranial CT scan revealed a large mass lesion in the right frontal subcortical region with central low density and peripheral high density areas, and small low density lesions in the right thalamic area and in the right posterior frontal region; ring enhancement was observed in the latter two lesions. On the second day of admission, she noted left-sided weakness which improved by corticosteroid treatment. On June 17, there was a sudden onset of left hemiparesis and a neurologic consultation was asked. Upon neurologic examination, she appeared somnolent but could understand verbal commands. She showed constructional apraxia, neglect of the left hemisphere, and anosognosia. Cranial nerves were unremarkable. Motor-wise, she showed flaccid left hemiplegia. Deep tendon reflexes were exaggerated on the left and the plantar response was extensor bilaterally. Nuchal stiffness was noted. Her cranial CT scan on June 17 revealed enlargement of the right frontal mass lesion. The subsequent course was complicated by DIC and progressive worsening of her consciousness. On June 18, she was comatose and pupillary light reflex was lost. She developed Cheyne-Stokes respiration and expired on that evening. The patient was discussed in a neurological CPC, and the chief discussant arrived at the conclusion that the patient had a primary adenocarcinoma in the lung with multiple metastases including the brain. The fulminant terminal course was ascribed to hemorrhage within the tumor and subsequent central type of transtentorial herniation. Opinions were divided regarding the cause of hemorrhage; some participants thought hemorrhage was caused by DIC. Post-mortem examination revealed an adenocarcinoma arising at the S6 segment of the left lung with multiple organ metastases. In the brain, a huge hemorrhagic metastasis was found in the right frontal lobe and a non-hemorrhagic metastasis in the right thalamic region. Probably, the size of the metastases influenced the occurrence of hemorrhage. The direct cause of the death was transtentorial herniation.
A representative sample of 55 mainstreamed 9-10-year-olds with hemiplegia were compared with all classmates on sociometric measures of popularity and friendship, and with 55 matched controls on measures of victimization. Children with hemiplegia were more rejected and less popular, had fewer friends, and were more often victimized; they were not more likely to be bullies themselves. These differences were not fully accounted for by group differences in teacher-estimated IQ and behaviour. Possible explanations range from neurologically determined deficits in mentalizing skills to peer prejudices about children with disabilities. The development of appropriate intervention strategies should be a high priority, particularly since peer problems not only result in current distress but also predict psychosocial problems in the future.
Magnetic resonance imaging (MRI), single photon emission computed tomography (SPECT) and magnetic resonance spectroscopy (MRS) were successively recorded in a 3-year-old girl with the acute hemiplegia syndrome. She was admitted to our hospital with complaints of fever, loss of consciousness and right side dominant clonic convulsions evolving into status epilepticus, and then recovered with sequelae of aphasia and right hemiparesis. Electroencephalography showed a generalized slow rhythm at the onset, and very low activities on the left hemisphere in the follow-up records. Brain CT and MRI revealed edema of the left hemisphere initially, followed by left side dominant brain atrophy. No cerebral vascular lesion was detected by magnetic resonance angiography. N-Isopropyl-[123I]-iodoamphetamine SPECT showed marked hypoperfusion of the left hemisphere accompanied by crossed cerebellar diaschisis. MRS at the initial stage detected decreased N-acetyl-aspartic acid and increased lactic acid signals in the bilateral hemisphere, which subsequently normalized only on the right side. These findings suggested brain damage and neural cell death in the left cerebral hemisphere, caused by acute encephalopathy. SPECT and MRS are useful new techniques to study the pathophysiology of the acute hemiplegia syndrome.
The usefulness of botulinum toxin A treatment when planning hand surgery in eight children with spastic hemiplegia was evaluated. The hand function of the children was assessed before and after treatment using a test battery consisting of quantitative and qualitative functional assessment. The results of preoperative botulinum treatment supported surgical intervention in four children and serial botulinum treatment in three children. In one child, the preoperative botulinum treatment provided no additional information. We conclude that preoperative botulinum A treatment in most children with spastic hemiplegia, for whom hand surgery is being considered, identifies the patients who would not benefit from the planned surgery or for whom the functional benefit would probably not outweigh the burden of surgical procedure and postoperative rehabilitation.
This light microscopic investigation of 15 Thoroughbred horses provided substantial evidence for the classification of equine laryngeal hemiplegia as a distal axonopathy. Morphologic and morphometric examinations were performed on resin embedded recurrent laryngeal nerves from control, subclinical and clinical laryngeal hemiplegic animals. In the latter group of animals some distal hindlimb nerves were also examined. A distally graded loss of myelinated fibres selectively affecting those of large diameter was demonstrated in both left and right recurrent laryngeal nerves. Morphologic evidence of similar pathological changes in long hindlimb nerves was also present. An explanation for the early involvement of the cricoarytenoideus lateralis muscle in the course of laryngeal hemiplegia, was offered by the demonstration of more large diameter fibres in the branch of the recurrent laryngeal nerve innervating it, thus making it more susceptible to the disease process.
Individual nerve fibres were isolated from the recurrent laryngeal and some distal hindlimb nerves, in an investigation of equine laryngeal hemiplegia. One hundred teased fibres were obtained from each of three sampling sites on both left and right recurrent laryngeal nerves, from 15 Thoroughbred horses. These fibres were graded descriptively and internode lengths measured. A distal distribution of pathology was demonstrated in all groups studied, but was most severe in the clinical group of horses. The predominant change was one of short thinly myelinated internodes interspersed amongst normally myelinated internodes, indicating remyelination of previously demyelinated areas of nerve fibre. Such pathological change was also reflected by the decreased mean internode length, and its increased variability associated with disease. However, it was determined statistically that these abnormal internodes were grouped along particular nerve fibres, rather than being randomly distributed between all nerve fibres. This is thought to indicate myelin sheath changes secondary to underlying axonal pathology. Thus it was concluded that the primary pathology was likely to be axonal in nature, while the high incidence of demyelination changes was a reflection of the chronic nature of the disease process. Thus, the distal distribution of pathology, the primary axonal involvement, the presence of changes in left and right recurrent laryngeal and distal limb nerves, all support the classification of equine laryngeal hemiplegia as a distal axonopathy.
Recent research on the muscular and nervous changes which occur in idiopathic equine laryngeal hemiplegia has indicated that many of the traditional concepts of the aetiology of this disease are erroneous. In light of the new knowledge gained, the various predispositions and possible causes of laryngeal hemiplegia are discussed, and it is suggested that the underlying mechanism of axonal damage in this neuropathy of horses may be related to abnormal energy metabolism in the axon.