Cancer and intestinal pseudo-obstruction.
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Biomedical subjects
Publications and source records attributed to O Lyon-Caen.
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Two anatomo-clinical cases of downward gaze palsy and one case of upward gaze palsy are reported. A tonic and intermittent downward gaze deviation is described. The supranuclear palsies of the downward gaze were related to paramedian lesions of the rostral mesencephalon; the lesions involved the rostral interstitial nucleus of the medial longitudinal fasciculus, the nucleus interstitial of Cajal, and/or their afferent and/or efferent pathways. The supranuclear palsy of the upward gaze was related to lesions of the posterior commissure. Tonic and intermittent downward deviation of gaze and ocular bobbing have opposed features. The former could be related to disinhibited reticular mesencephalic neurones activated by vestibular inputs. Tonic upward deviation of gaze is also related to a vestibulo-ocular reflex. In this case, partial or total damage of the nucleus of Cajal, and/or its input and/or its output fibers appears to have a critical role.
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The clinical and neuropathological findings in 28 cases of paramedian thalamic and midbrain infarcts are reported. The 4 instances of unilateral paramedian thalamic infarct were characterized by mood and behavioral changes, limitation of the infarct to the center of the anatomical paramedian territory, and symmetrical configuration of the paramedian thalamic arteries. Basilar artery occlusion was found in 1 patient. The 5 cases of bilateral paramedian thalamic infarcts were characterized by disturbances of consciousness and behavior, extension of the infarct (to the mammillothalamic tracts in 4 cases, the red nuclei in 3, and the hypothalamus in 2), and a variable paramedian thalamic arterial pattern. The arterial pattern was symmetrical in 2 cases, asymmetrical in 1, and unilateral in 1. The basilar artery was occluded in 1 case, the basilar communicating and posterior cerebral arteries in 1, and a third patient had occlusion involving an aneurysm of the basilar artery. The 19 patients with paramedian thalamopeduncular infarcts had marked disturbances of consciousness (hypersomnia, deep coma, akinetic mutism) associated with ocular motility changes. Later, abnormal movements--always delayed--and memory disturbances were observed in some. Thalamic changes were restricted to beh paramedian territory in only 3 cases. The arterial pattern was symmetrical in 5. The basilar and posterior cerebral arteries were occluded in 4 patients each. Paramedian infarcts were rarely found as isolated lesions and were always bilateral when there was only one arterial pedicle. The paramedian thalamic pedicle can supply the polar thalamic territory.
Four cases of angioimmunoblastic lymphadenopathy associated to peripheral neuropathy are described. The neuropathy was mixed, sensory and motor, more or less extensive, always asymetrical. In two cases, the clinical symptomatology and the clinical course were very peculiar, characterized by sensory disorders of a precise topography, circumscribed and sometimes suspended and by a relapsing and remitting course. In the third case, the neurological signs were acute and rapidly extensive with mandatory respiratory assistance. In this case, death occurred after a few weeks and the exact diagnosis was only attained at post-mortem examination. In the fourth case the neuropathy was very painful but the course was slow. In all four cases marked and extensive pain was present prior to the neurological disorders. Electrophysiological abnormalities were a constant feature with a marked slowing down of nerve conduction velocity. CSF was normal at the beginning in one case but was otherwise markedly pathological with an increased number of cells due to a large number of lymphocytes ranging from 6 to 40 cells while protein ranged from 60 to 160 mg per 100 ml. Nerve and muscle biopsies were non specific, i.e. neurogenous muscular atrophy and demyelination, except in case n. 4 where specific angioimmunoblastic lymphadenopathy infiltrates were present both in nerve and muscle. In cases 1 and 3 a non specific lymphohistiocytic infiltrate was present in spinal roots and meninges. Corticotherapy was used and efficient in two cases. These data are compared with a review of the literature. Since 1976, 7 cases of angioimmunoblastic lymphadenopathy associated to peripheral neuropathy have been reported. Clinical, electrophysiological and biological features are similar. Only one case underwent a post mortem examination of the central nervous system: a non specific lymphocytic infiltration in the spinal roots and meninges was mentioned. The role of the dysproteinemia associated with the AIL in the occurrence of the neuropathies is discussed. It remains a possible factor only. The role of a massive specific localization of the pathological process is well established in only one case (case 4). Such localization in lymphomas are not unusual. In 2 of our cases as well as in 2 from the literature the pathological findings are non specific: mild lymphoplasmocytic infiltrates of spinal roots and meninges. Those lesions are similar to neuropathies associated to non metastasizing neoplasms or malignant hemopathies.
Two anatomo-clinical cases of a necrotic form of demyelinating disease are reported. The disease occurred in two women, had a late onset (patient were about 50 years old) and had a relapsing-remitting course during more than 10 years. The CSF displayed a high protein level over 125 mg/100 ml whereas the gamma-globulin level was normal. The anatomical study found symmetrical cavitations involving both hemispheres and optic tracts with clear-cut limits. Axons and myelin were both destroyed, only the vascular network being partially spared. At the lesion's border-line mononuclear cell infiltrates as well as some phagocytes with sudanophilic inclusions were found. The scarcity of the compound granular corpuscules suggest an old pathological process. A narrow zone of myelin-axonal dissociation was also observed. Astrocytic proliferations was unimportant. Blood vessels were normal. In one case plaques of multiple sclerosis were found in the spinal cord. Those two cases are unusual forms of a diffuse disseminated sclerosis: multiple sclerosis and Schilder's disease are considered as two anatomo-clinical variants of the same pathological process. The observed necrotic lesions are different from the acute necrotic forms of multiple sclerosis as the latter have rapidly developed. The long lasting course of the disease, over 10 years, allowed a complete resolution of the lesions explaining the cavitations. The late onset of the disease and the CSF high protein level are pointed out. The significant of the high protein level and normal gammaglobulin level in the CSF is discussed.
Multiple Sclerosis (MS) cases found at autopsy in patients who had died from other diseases and in whom no sign or symptom could be related to MS are called "asymptomatic". Three cases are reported. The first patient was a 62 year old man who presented with a slowly progressive disturbance of gait, incontinence and deterioration of intellectual function. A falx meningioma was surgically removed. The patient died 3 years later with an acute respiratory illness. Examination of the brain disclosed evidence of the operation and numerous old plaques disseminated through the cerebral hemispheres (centrum semi-ovale, periventricular regions, internal thalamus and junction between cortex and white matter) and in the brain stem. The second case, a 77 year old woman with diabetes mellitus and hypertension, presented with cortical blindness and disturbances of memory of acute onset. She died one year later. Examination of the brain showed multiple infarcts involving the territories of both posterior cerebral arteries and the left middle cerebral artery. Numerous old plaques were seen in the periventricular regions, in the corpus callosum and in the left middle cerebellar peduncle. The third case, a 60 year old woman with mitral and aortic stenosis, presented with cortical deafness and transient right hemiparesis. She died 5 years later. Brain examination showed infarcts involving both middle cerebral artery territories. There was also many old plaques in the periventricular areas, thalamus, internal capsule, centrum semi-ovale, brain stem and right nucleus dentatus. In the 3 cases, the optic tracts were normal. The spinal cord, examined only in the first case, was also normal. The asymptomatic character of these MS cases can be explained first by the location of the plaques and the lack of spinal cord and optic tract involvement. It could also be due to the small size of the plaques and to axonal preservation. Such features are rare since our 3 observations have been selected from a pathological collection of 125 MS cases and 9,300 general neuropathological records. Six other cases have been previously reported by other authors.
A 67 years old man was admitted on July 1979 for nausea, dysphagia and rectal pain. At age 64 he had undergone radiotherapy on the lower lip for an epidermoid carcinoma. He remained then healthy. His medical history was negative with the exception of chronic bronchitis. He had never been exposed to toxic agents or drugs and had never left Europe. A few days after admission he suffered acute intestinal obstruction but at laparostomy no etiology was found. At the same time the patient complained of pain in all four limbs and he was found to have diffuse wasting of muscles, areflexia and distal sensory loss. No sign of dysautonomia was present. Physical examination was negative with the exception of a cervical lymphadenopathy. The lymph node biopsy showed an undifferentiated metastatic carcinoma. Negative investigations included: blood cells count; serum ionogram and immunoelectrophoresis; thyroid function tests; serological test for Chagas' disease. The following abnormalities were found: ESR: 55-105; CSF protein: 145 mg/100 ml and 1 cell mm3; whole blood folic acid: 1,7 mg/ml; Hbs antigen was present in blood; EMG showed evidence of denervation but motor conduction velocities were normal. By September the patient's weakness had increased and complete intestinal obstruction persisted. At oesophageal, gastric and duodenal fibroscopy no contraction was visible, and biopsies were negative. The patient died of peritonitis on October 5th, 1979. At necropsy peritonitis secondary to multiple perforation of the large bowel was found. No recurrence of the lip carcinoma or metastase or evidence of a primary carcinoma was found. Light microscopy showed no evidence of amyloidosis or scleroderma. Examination of the alimentary tract showed abnormalities restricted to the myenteric plexuses which varied from one level to another. In the small bowel there was hyperplasia of the smooth muscle and the myenteric plexuses were enlarged by marked proliferation of Schwann cells. Severe neuronal loss and nodules of Nageotte were also noted. Schwann cells proliferation was less marked in the stomach and large bowel. Lympho-histiocytic infiltration strictly confined to the region of the myenteric plexuses was present in oesophagus, stomach, large bowel and rectum. Mild chronic inflammatory lesions were also found in anterior and posterior spinal roots and semi-lunar ganglia. The striking feature of this case is the association of an undifferentiated carcinoma and a polyradiculoneuritis with a complete alimentary tract palsy of rapid onset, secondary to lesions restricted to the myenteric plexuses. The low folate level was insufficient to explain the neuropathy. Investigations showed no evidence of the usual causes of intestinal pseudo-obstruction: muscular, dysautonomic, toxic, plexic (idiopathic, familial, inflammatory), Chagas' disease). The clinical course, the pathological pictures of the alimentary tract and spinal roots and the association with a carcinoma suggest that our case may represent a paraneoplastic syndrome...
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X ray dynamic study of cerevical spine movements in 12 patients with neurological impairment has shown an abnormal mobility between two vertebrae in the anterior or posterior direction. This abnormal mobility which has been called functional dislocation, is situated usually over major discarthrosic lesions rather than under. This dislocation, which appears during voluntary and automatic movements of the head and neck has been qualified chronic. A discectomie through an anterior surgical approach and a bony fusion of vertebral bodies without any graft at the dislocation site lead to 10 good results. 2 failures have been imputed to the fact that there was a 10 years evolution of a tetraplegia before operation. The pathogenesis of chronic functional dislocation of the cervical spine is discussed with regard to compression and stretching of the spinal cord, roots and arteries of both. Traumatism of vertebral arteries during dislocation remain under discussion.
Several observations suggest that retroviral infection is involved in the pathogenesis of the human demyelinating disease multiple sclerosis (MS). First, lymphadenopathy-associated virus/human T-lymphotropic virus type III (LAV/HTLV-III), the agent of acquired immune deficiency syndrome (AIDS), has been shown to be neurotropic in man. Second, the genetic organization of the lentivirus visna, which causes a chronic demyelinating disease of sheep, closely resembles that of LAV/HTLV-III. Recently, Koprowski and colleagues reported that MS is associated both with raised levels of circulating antibodies to HTLV-I and with the presence of HTLV-I-specific RNA within cell lines derived from the cerebrospinal fluid (CSF). Here we report that no HTLV-I-like or LAV/HTLV-III-like sequences can be detected, by in situ hybridization, in central nervous system (CNS) tissues from MS patients, and that nonspecific HTLV-I-like signal in peripheral blood mononuclear cells or in CSF cell lines is characteristic of MS. Furthermore, enzyme-linked immunosorbent assay (ELISA) analysis of circulating and CSF antibodies for HTLV-I reactivity fails to distinguish between MS and control groups.
MR T2 Weighted sequences on the brain demonstrate disseminated "high signal zones" (HSZ) in patients with Multiple Sclerosis; these morphological alterations are corresponding to the plaques. From the very beginnings of MR in 1981, everybody recognizes the main importance of this fact. MR appears as the most sensible exploration in patients with M.S. But the signal alteration is not specific; the clinical considerations and the evolution are requested. The aim of this work is to give a reference tool for evolutive evaluation of the disease. A work station with a specially developed software are presented. The HSZ thresholding is partially automatic. The edition of a cerebral mapping is developed. These results are discussed.
It appears from a study of 100 cases of acute cerebral disease that electroencephalography is valuable as part of the diagnosis strategy and not only to establish the correct final diagnosis. This examination therefore plays a non-negligible role in neurological practice. In a number of diseases it provides information that no other examination can provide, being a dynamic, functional method of brain tissue analysis.
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