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PubMed1983

Mesencephalic and bulbar reticular influences on somatosensory cortical neurons: short- and long-latency effects.

Somatosensory cortical neurons were intracellularly and extracellularly recorded in cats encéphale isolé, and after acute lesions of midthalamic nuclei or after chronic hemisection of the brain stem at the pretrigeminal level. Intracellular recordings showed postsynaptic facilitatory and inhibitory effects at very low latency by stimulating both the mesencephalic (MRF) and bulbar reticular formation (BRF). Inhibitory effects dominated by stimulating the BRF. Neither midthalamic lesions nor pretrigeminal hemisection changed the quality of latency of postsynaptic responses. Extracellular recordings revealed long-latency inhibition of discharge following MRF stimulation after midthalamic lesion. In these experimental conditions long-latency BRF effects were abolished. No differences were found in responses of pyramidal tract (PT) or non-PT neurons during BRF and MRF stimulation. The results are discussed on the basis of a possible extrathalamic differential reticular control, from caudal and rostral brain stem, of somatosensory cortical neurons.

Animals↗
PubMed1985

Relationship of periodic movements in sleep (nocturnal myoclonus) and the Babinski sign.

To obtain a comprehensive clinical description of periodic movements in sleep, the first 11 videotaped movements of nine patients were studied. These leg movements were characterized by active dorsiflexion of the ankle (91%), dorsiflexion and fanning of the small toes (82%), and dorsiflexion of the great toe (72%). Partial flexion of the knee and hip occurred in 28%. Simultaneous dorsiflexion of the ankle and small toe was almost always the initial change, either preceding or occurring simultaneously with extension of the great toe. Knee and hip flexion almost always followed foot movements. Tonic and/or clonic movements, usually about the ankle, occurred in 75%; plantar flexion of the ankle occurred in 21% at the end of a leg movement. Periodic movements in sleep were thus characterized on detailed videographic analysis by movements similar to the Babinski response. Since both the normally occurring nocturnal Babinski response and periodic movements in sleep are also almost entirely NREM related, the author proposes that periodic movements in sleep are due to the NREM loss of supraspinal inhibitory influences on the pyramidal tract and that the characteristic foot and leg movements are Babinski-type responses secondary to this.

Adult↗
PubMed1986

Somatosensory and brainstem auditory evoked responses in sleep-related periodic leg movements.

The pathophysiological mechanisms of sleep-related periodic leg movements (sPLM) and restless legs syndrome are unknown. Evoked potentials have been demonstrated to be abnormal in a variety of episodic movement disorders. In the present study, mixed nerve somatosensory and brainstem auditory evoked responses were examined in patients with polysomnographically documented sPLM who also had restless legs. Normal lower extremity (posterior tibial nerve stimulation) and upper extremity (median nerve stimulation) somatosensory evoked responses were recorded in a group of 10 patients with documented sPLM. Brainstem auditory evoked responses also were normal. These findings do not provide any evidence for a primary afferent sensory disturbance and indirectly support a recently forwarded hypothesis that sPLM is a reflection of suppression of descending inhibitory influences on pyramidal tract function.

Adult↗
PubMed1989

Neurological disorders in AIDS and HIV disease in the northern zone of Tanzania.

This study presents the main clinical findings on 200 AIDS patients at Kilimanjaro Christian Medical Centre in the northern zone of Tanzania, with detailed neurological findings on 135 out of 200 cases and 53 controls. Results show that 21 out of 200 (10.5%) had an obvious focal neurological disorder, including cranial nerve palsies, hemiparesis and paraparesis. Ninety-seven out of 135 (72%) had less obviously detectable neurological disorders, versus 36% of controls (P less than 0.005). Most frequent were AIDS dementia complex (54%), retinopathy (23%), areflexia (21%), pyramidal tract signs (19%) and tremor and incoordination (19%). Frontal lobe release signs (FLRS) were found in 103 out of 135 (76%) patients, versus 36% of controls (P less than 0.005). Advanced and terminal AIDS cases were more likely to have neurological disorders than early AIDS patients. A further study on 87 non-AIDS patients with acute unexplained neurological disorders showed 10 out of 87 to be HIV seropositive. Three case studies are presented. This study suggests that neurological disorders are among the main clinical features of AIDS and HIV disease in Africa.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

Diffusion magnetic resonance imaging in infantile neuroaxonal dystrophy.

A 7-month-old girl with infantile neuroaxonal dystrophy is reported. In diffusion MRI, the pyramidal tracts and dentate nuclei had high signal on b = 1,000 s/mm2 images and low apparent diffusion coefficient (ADC) values. This pattern likely reflected the presence of abnormal (dystrophic) axons with restricted mobility of water molecules. A reverse pattern was evident in the cerebellar cortex with high ADC values. This was likely a reflection of dysmyelination or lack of myelination.

Brain↗
PubMedDate not supplied

Nonketotic hyperglycinemia: diffusion magnetic resonance imaging findings.

We report about a boy with nonketotic hyperglycinemia who was studied at 15 days of life with a follow-up examination at age 6 months. Magnetic resonance (MR) imaging revealed progressive atrophy, callosal thinning, and delayed myelination. Glycine peaks were shown by proton MR spectroscopy at 3.56 ppm with a long echo time (TE, 135 milliseconds; TR, 1500 milliseconds). Echo-planar diffusion MR imaging (TR, 5700 milliseconds; TE, 139 milliseconds) at 15 days of life revealed high-signal lesions in the pyramidal tracts, middle cerebellar pedicles, and dentate nuclei on b = 1000 s/mm2 images associated with low apparent diffusion coefficient (ADC) values. By age 6 months, the lesions became more prominent on b = 1000 s/mm2 images with lower ADC values. Diffusion MR imaging findings likely reflected the histopathologic changes of the disease which consisted of spongiosis of the myelinated brain tissue due to myelin vacuolation.

Atrophy↗
PubMed1991

Human T-lymphotropic virus type 1-associated myelopathy and primary sclerosing cholangitis.

We report the first case of human T-lymphotropic type 1-associated myelopathy (HAM) linked with primary sclerosing cholangitis (PSC). The patient, a 44-year-old woman, also suffered from ulcerative colitis and polyarthritis. Two years and nine months after the clinical onset of PSC, the coexistence of HAM was shown by neurological manifestations characterized by slowly progressive symmetrical myelopathy, predominantly involving pyramidal tracts, and positive antibodies to human T-lymphotropic virus type 1 in serum as well as in cerebrospinal fluid.

Adult↗
PubMed1979

Pathology of Shy-Drager syndrome.

In four patients with the Shy-Drager syndrome, detailed pathological findings in the central nervous system are described. All four patients had striatonigral degeneration, olivopontocerebellar atrophy, pyramidal tract degeneration and ventral horn cell loss. Along with the multisystem degeneration, there was widespread loss of thoracolumbar autonomic neurons, which was demonstrated by comparative cell counts of the intermediolateral horns in two of the four patients. In all four patients, autonomic nuclei of the sacral cord, particularly the Onuf's and intermediolateral nuclei, were severely affected and diffuse cell loss in the nuclei seems to account for disordered bladder, rectal and sexual functions in Shy-Drager syndrome.

Aged↗
PubMed1991

Ubiquitin in motor neuron disease: study at the light and electron microscope.

Several neurodegenerative diseases, including motor neuron disease (MND), are characterized by formation of abnormal cytoskeleton-derived inclusions which contain ubiquitin (Ubq). We have studied the distribution of Ubq in 26 cases of MND with light and electron microscopic immunocytochemistry. Ubiquitin-positive inclusions were found in neurons of anterior horns in most cases of amyotrophic lateral sclerosis (ALS) but were not present in other forms of MND. Ubiquitin immunoreactivity was observed in 10-15 nm intraneuronal filaments, which were not stained by antibodies to neurofilaments, and on dense bodies of dystrophic neurites throughout the neuropil of anterior horns and pyramidal tracts. Data analysis showed a trend toward lower percentage of Ubq-positive neurons in cases with longer duration of illness or lower number of neurons. A high percentage of Ubq-positive inclusions occurred in cases with an aggressive clinical course, suggesting that ubiquitination takes place at early stages of the disease.

Adult↗
PubMed1997

Clinical and neuropathological study of six patients with spastic paraparesis associated with HTLV-I: an axomyelinic degeneration of the central nervous system.

Between 1990 to 1994, 6 TSP/HAM patients, 3 women and 3 men with an average age of 57.1 years (39 to 76 years old), who died in the Salvador Hospital were submitted to postmortem examination. The mean time of paraparesis was 7 years (3 to 17 years), and 2 patients had pseudobulbar signs. Three cases had macroscopic atrophy of the spinal cord. Histologically, all cases had lesions in the pyramidal tracts and 4 cases showed somatotopic lesions of the Goll's tracts which followed a "dying back" ascendant and descendant distribution, respectively. In 2 cases, both of which had intellectual impairment, demyelination of the subcortical and parathalamic areas was observed without U fiber involvement. Abnormal vessels with gross thickening of the adventitia, many of them with lymphocytic cuffs, were seen everywhere, especially in the spinal cord, brain stem, midbrain and meninges, but no relation between these findings and the parenchymal lesions was observed. Also, in the cases with posterior column involvement, neuronal changes and proliferation of satellite cells in the dorsal ganglia were found. All cases showed histological sialoadenitis and none had inflammatory muscle changes. We conclude that the lesions affected the neuraxis in a systemic axial fashion as in degenerative diseases, and did not seem to be secondary to vascular or inflammatory abnormalities.

Adult↗
PubMed1992

Erroneous diagnosis within the cranial vault.

The majority of pediatric neoplasias of the brain are midline growths in the posterior fossa. These mass lesions lead to obstruction of cerebrospinal fluid circulation and cause increased intracranial pressure. Affected children typically present with insidious complaints of headache and vomiting. Ataxia, cranial nerve palsies, or pyramidal tract signs may be present at the time the diagnosis is entertained. In the reports describing pathognomonic clinical features of posterior fossa tumors, an accelerated presentation with minimal prodromal events has not been emphasized. This report details the case of a child with a cerebellar medulloblastoma who presented with abrupt onset of fever, nuchal rigidity, and altered mental status. Emergency department misdiagnosis occurred.

Acute Disease↗
PubMed1990

Spongiform encephalopathies: the physician's responsibility.

The spongiform encephalopathies encompass several diseases affecting humans and animals. In the United States, the most common of these disorders in humans is Creutzfeldt-Jakob disease. The most frequent manifestations include dementia, pyramidal tract signs, and extrapyramidal movement disorder. Several clinically distinct syndromes can be identified. Often the diagnosis is confused with other forms of dementia, and the only definitive method for establishing the diagnosis is autopsy evaluation of brain tissue. Unfortunately, since the recognition of the infectious etiology of Creutzfeldt-Jakob disease, fear has often unreasonably interfered with clinical care and autopsy evaluation of affected patients. In actuality, because of the low and restricted infectivity of the responsible agent, affected individuals present minimal risks to clinical caretakers, and handling of patient specimens is not dangerous if appropriate precautions are taken. These precautions are well established, and physicians and other health care workers should not refuse care of appropriate evaluation (including autopsy) to individuals with suspected Creutzfeldt-Jakob disease.

Aged↗
PubMed1998

Intravascular malignant lymphomatosis with neurologic presentation: factors facilitating antemortem diagnosis.

Intravascular malignant lymphomatosis (IML) is a rare disorder of small and medium size vessels that frequently goes undiagnosed until the time of autopsy. The clinical courses of two such patients were examined to determine factors that would facilitate antemortem diagnosis. Both patients had mental status changes, pyramidal tract signs, and peripheral neuropathy. Despite postmortem evidence of widespread lymphocytic invasion of vessels throughout the body including peripheral and central nervous systems, neuroimaging studies, cerebrospinal fluid analysis, peripheral blood studies, and bone marrow biopsy failed to reveal diagnostic evidence of the underlying neoplastic process. Although markedly abnormal, nerve conduction studies were nonspecific. Familiarity with IML and its consideration in the differential diagnosis when central and peripheral nervous system dysfunction occur concurrently may guide the physician to tissue biopsy facilitating antemortem diagnosis and institution of appropriate therapy.

Aged↗
PubMed1991

Magnetic stimulation of motor cortex and motor roots for painless evaluation of central and proximal peripheral motor pathways. Normal values and clinical application in disorders of the lumbar spine.

Magnetic stimulation of the motor cortex, motor roots, and proximal nerve trunks was performed in 46 healthy adults and in 73 consecutive patients with disorders of the lumbar spine. In combination with neurography and F-wave recordings, the fractionated stimulation of the motor pathways allowed calculation of conduction times of the pyramidal tract fibers, of the motor roots (ie, caudal fibers), and of the motor fibers of the lumbosacral plexus. Normal values for motor conduction times to the quadriceps, anterior tibial, and extensor digitorum brevis muscles were established. Patients had clinical and radiologic diagnoses of spinal stenosis (n = 43) and nerve root compression syndromes (n = 30). Motor conduction times to lower limb muscles were significantly delayed (above mean normal value +/- 2 x SD) in 65% of the patients with spinal stenosis and 50% of the patients with nerve root compression syndromes. Conduction slowing could be localized within the motor root and caudal fiber segment of the motor pathways in 80% of the patients in whom F-waves could be recorded. This method can be used to verify, quantify, and locate lesions of the motor pathways in conditions such as compression of the spinal cord, the caudal fibers (spinal stenosis), or the motor root passing through the intervertebral canal.

Adult↗
PubMed1995

Babinski and Babinski sign.

Babinski's sign probably is the best known neurologic eponym, referring to dorsiflexion of the great toe with or without fanning of the other toes and withdrawal of the leg. This follows plantar stimulation in patients with pyramidal tract dysfunction. Although the plantar reflex already had been described, Babinski--a French neurologist of Polish descent and a pupil of Charcot--was the first to differentiate between a normal and pathologic response of the toes and recognize its clinical implication. Despite the continuing controversy over its pathophysiologic interpretation, the clinical utility of Babinski's sign remains unchanged almost 100 years after its description.

Eponyms↗
PubMed2001

Non-progressive mental retardation and peripheral neuropathy in a mother and her son.

The association of facial dysmorphism, moderate mental retardation and peripheral neuropathy was observed in a mother and her son. The son also has pyramidal tract involvement in the lower limbs. Although exactly the same association has not been described previously, it seems probable that it results from variable expression of a dominant gene defect.

Adolescent↗
PubMed2004

The effects of occupational exposure to chlorpyrifos on the neurologic examination of central nervous system function: a prospective cohort study.

Questions persist about adverse effects such as impaired cognition and attention, incoordination, spasticity, or parkinsonism from chronic, low-level exposures to organophosphate (OP) compounds. In a prospective cohort study, we evaluated chlorpyrifos-manufacturing workers and a referent group on 2 occasions, 1 year apart, to determine whether occupational exposure to chlorpyrifos produced clinically evident central nervous system (CNS) dysfunction. Chlorpyrifos subjects had significantly higher TCP excretion and lower average BuChE activity than referents in a range in which physiological effects on B-esterases exist. Few subjects had neurologic symptoms or signs, and there were no significant group differences in terms of signs at baseline or second examinations. Chronic chlorpyrifos exposure produced no clinical evidence of cortical, pyramidal tract, extrapyramidal, or other CNS dysfunction among chlorpyrifos subjects compared with referents, either at baseline or after 1 year of additional chlorpyrifos exposure.

Adult↗
PubMed2004

Differential localization of neurons susceptible to enterovirus 71 and poliovirus type 1 in the central nervous system of cynomolgus monkeys after intravenous inoculation.

Poliovirus and enterovirus 71 (EV71) are both neurotropic enteroviruses that cause serious neurological diseases, such as poliomyelitis and encephalitis. The neurovirulence of EV71 in cynomolgus monkeys was demonstrated previously by intraspinal inoculation. In this study, an improved simian model of EV71 infection was established by using intravenous inoculation, which revealed clinical and neuropathological similarities between this model and human cases of encephalitis. Experimental EV71 infection induced direct neurological manifestations, such as tremor, ataxia and brain oedema, but not non-neurological complications, such as pulmonary oedema and cardiac failure. Using this model of EV71 infection, the neurotropic characteristics of the prototype strains of EV71 and poliovirus type 1 (PV1) were compared. Three monkeys were inoculated intravenously with 10(5.5) TCID50 EV71 and all developed neurological disease signs within 4-6 days of inoculation. However, after inoculation with 10(5.5) TCID50 PV1 strain OM1 (PV1-OM1), the major manifestation was flaccid paralysis, starting from the lower limbs 6-9 days post-inoculation. Histopathological and virological analyses of moribund monkeys revealed that disseminated EV71 infection was characterized by severe panencephalitis involving both the pyramidal and extrapyramidal systems. In contrast, the lesions induced by PV1-OM1 were mainly restricted to the pyramidal tract, particularly the spinal motor neurons, thalamus and motor cortex. In conclusion, neuropathological involvement in this model correlated well with the apparent differences in neurological disease induced by EV71 and PV1-OM1. Thus, intravenous inoculation with EV71 is an excellent model to study the neuropathology of EV71 and to evaluate candidate vaccines and potential antiviral agents.

Animals↗