Changes in Diffusion Metrics of the Red Nucleus in Chronic Stroke Patients With Severe Corticospinal Tract Injury: A Preliminary Study

OBJECTIVE: To explore plastic changes in the red nucleus (RN) of stroke patients with severe corticospinal tract (CST) injury as a compensatory mechanism for recovery of hand function. METHODS: The moderate group (MG) comprised 5 patients with synergistic hand grasp movement combined with limited extension, and the severe group (SG) included 5 patients with synergistic hand grasp movement alone. The control group (CG) included 5 healthy subjects. Motor assessment was measured by Motricity Index (MI). Diffusion tensor imaging was analyzed using fractional anisotropy (FA) and radial diffusivity (RD) in the individual regions of interest (ROIs)—bilateral internal capsule and anterior pons for CST injury and bilateral RN for rubrospinal tract (RST) injury. RESULTS: The SG showed a significantly lower MI score than the MG mainly due to differences in hand subscores. Significantly reduced FA was observed in both MG and SG compared with CG, while SG showed increased MD and RD in the affected ROIs of CST, and increased FA on the unaffected side compared with CG. However, in the RN ROI, a significantly increased FA and decreased RD on the unaffected side similar to the affected side were found only in the SG. The relative index of FA was lower and RD in SG was higher than in CG in RST. CONCLUSION: The diffusion metrics of RST showed changes in patients with severe CST injury, suggesting that RST may play a role in the recovery of hand function in patients with severe CST injury.

Neuroradiological and Neurophysiological Characteristics of Patients With Dyskinetic Cerebral Palsy

OBJECTIVE: To investigate neuroradiological and neurophysiological characteristics of patients with dyskinetic cerebral palsy (CP), by using magnetic resonance imaging (MRI), voxel-based morphometry (VBM), diffusion tensor tractography (DTT), and motor evoked potential (MEP). METHODS: Twenty-three patients with dyskinetic CP (13 males, 10 females; mean age 34 years, range 16-50 years) were participated in this study. Functional evaluation was assessed by the Gross Motor Functional Classification System (GMFCS) and Barry-Albright Dystonia Scale (BADS). Brain imaging was performed on 3.0 Tesla MRI, and volume change of the grey matter was assessed using VBM. The corticospinal tract (CST) and superior longitudinal fasciculus (SLF) were analyzed by DTT. MEPs were recorded in the first dorsal interossei, the biceps brachii and the deltoid muscles. RESULTS: Mean BADS was 16.4+/-5.0 in ambulatory group (GMFCS levels I, II, and III; n=11) and 21.3+/-3.9 in non-ambulatory group (GMFCS levels IV and V; n=12). Twelve patients showed normal MRI findings, and eleven patients showed abnormal MRI findings (grade I, n=5; grade II, n=2; grade III, n=4). About half of patients with dyskinetic CP showed putamen and thalamus lesions on MRI. Mean BADS was 20.3+/-5.7 in normal MRI group and 17.5+/-4.0 in abnormal MRI group. VBM showed reduced volume of the hippocampus and parahippocampal gyrus. In DTT, no abnormality was observed in CST, but not in SLF. In MEPs, most patients showed normal central motor conduction time. CONCLUSION: These results support that extrapyramidal tract, related with basal ganglia circuitry, may be responsible for the pathophysiology of dyskinetic CP rather than CST abnormality.

Neuroradiological and Neurophysiological Characteristics of Patients With Dyskinetic Cerebral Palsy

OBJECTIVE: To investigate neuroradiological and neurophysiological characteristics of patients with dyskinetic cerebral palsy (CP), by using magnetic resonance imaging (MRI), voxel-based morphometry (VBM), diffusion tensor tractography (DTT), and motor evoked potential (MEP). METHODS: Twenty-three patients with dyskinetic CP (13 males, 10 females; mean age 34 years, range 16-50 years) were participated in this study. Functional evaluation was assessed by the Gross Motor Functional Classification System (GMFCS) and Barry-Albright Dystonia Scale (BADS). Brain imaging was performed on 3.0 Tesla MRI, and volume change of the grey matter was assessed using VBM. The corticospinal tract (CST) and superior longitudinal fasciculus (SLF) were analyzed by DTT. MEPs were recorded in the first dorsal interossei, the biceps brachii and the deltoid muscles. RESULTS: Mean BADS was 16.4+/-5.0 in ambulatory group (GMFCS levels I, II, and III; n=11) and 21.3+/-3.9 in non-ambulatory group (GMFCS levels IV and V; n=12). Twelve patients showed normal MRI findings, and eleven patients showed abnormal MRI findings (grade I, n=5; grade II, n=2; grade III, n=4). About half of patients with dyskinetic CP showed putamen and thalamus lesions on MRI. Mean BADS was 20.3+/-5.7 in normal MRI group and 17.5+/-4.0 in abnormal MRI group. VBM showed reduced volume of the hippocampus and parahippocampal gyrus. In DTT, no abnormality was observed in CST, but not in SLF. In MEPs, most patients showed normal central motor conduction time. CONCLUSION: These results support that extrapyramidal tract, related with basal ganglia circuitry, may be responsible for the pathophysiology of dyskinetic CP rather than CST abnormality.

[Effects of tobacco on antipsychotic treatments and their extrapyramidal symptoms in schizophrenia]

The prevalence of cigarette smoking is significantly higher among patients with schizophrenia than in the general population. Several authors explained this excess of smoking by the self-medication hypothesis. It suggests that patients with schizophrenia smoke to reduce psychotic symptoms or antipsychotic side effects. In this study, we aimed to evaluate the prevalence of tobacco consumption in patients with schizophrenia and to test if smoking reduces psychotic and extra-pyramidal symptoms. We included 115 patients with schizophrenia [DSM IV] treated with conventional antipsychotics. We assessed psychotic symptoms with the Positive and Negative Syndrome Scale [PANSS] and extrapyramidal symptoms with the Simpson-Angus scale. Prevalence of smoking was 60% [80% in men and 22.5% in women]. The majority of them started their consumption before their illness. Smokers and non-smokers had similar rates of psychotic and extrapyramidal symptoms with comparable doses of antipsychotics and anticholinergic agents which were prescribed for similar durations. In this study, patients with schizophrenia smoke a lot for reasons other than reducing psychotic or extrapyramidal symptoms

Isquemia de ganglios basales por intoxicación de heroína y cocaína aspiradas / Basal ganglia ischemia by aspirated heroin and cocaine intoxication

La cocaína es una de las drogas de abuso más usadas en el mundo y se relaciona con la aparición de eventos isquémicos y hemorrágicos en el sistema nervioso central y cardiovascular. Esto se debe a diversos factores tales como: vasoespasmo, vasculitis cerebral, incremento de la agregación plaquetaria, cardioembolismo y urgencias hipertensivas asociadas con la alteración de la autorregulación cerebral. Se describe el caso de un paciente que ingresa a la Clínica Universitaria Bolivariana con un cuadro de intoxicación aguda por cocaína y heroína aspiradas. Presentó infarto agudo de miocardio con elevación del segmento ST en las derivaciones V1, V2 y V3, aumento de troponinas, hipomagnesemia, hipercalemia, hipocalcemia, acidosis mixta, neumonía aspirativa, depresión del estado de conciencia con respiración superficial, cianosis y síndrome de abstinencia, que se manejó con haloperidol en unidad de Cuidados intensivos. Posteriormente, el paciente presentó un cuadro de extrapiramidalismo secundario a este tratamiento, por ello se inicia desmonte del haloperidol y se administra biperideno y bromocriptina sin remisión total de los síntomas. Finalmente, se evidenció, por resonancia magnética nuclear, isquemia de ganglios basales. El objetivo de este reporte es describir las manifestaciones clínicas presentadas por el paciente asociadas con el consumo atípico de estas dos drogas, así como hacer una aproximación al manejo terapéutico de esta patología.

Comparison of Intramuscular Olanzapine and Intramuscular Haloperidol in Treatment of Acute Agitation in Patients of Schizophrenia.

Objectives: To determine the antipsychotic efficacy and extra pyramidal safety of intramuscular olanzapine and intramuscular haloperidol during the first 24 hours of treatment of acute agitation in schizophrenia. Methods: Patients (n = 29) with schizophrenia were randomly allocated to receive one to three injections of intramuscular olanzapine (10 mg, n =14), intramuscular haloperidol (10 mg, n = 14) over a 24-hour period. Agitation was measured with the excited component of the positive and negative symptom scale (PANSS) and agitation behavior scale (ABS). Results: After the first injection, IM olanzapine was comparable to IM haloperidol for reducing mean changes in scores from baseline on excited component of PANSS at 2 hours to ( -13.08 olanzapine, -8.07 haloperidol ) and at 24 hours (-9.86 olanzapine, -8.07 haloperidol ). Mean changes in the scores of ABS scale from baseline was at 2 hours (-9.78 olanzapine, -8.54 haloperidol) and at 24 hours (-6.14 olanzapine, -6.6 haloperidol). Patients treated with IM olanzapine had significantly fewer incidence of treatment emergent Parkinsonism (0% olanzapine versus 6.66% haloperidol, p = 4.55), no patient had akathisia with olanzapine as compared to 13.33% of patients with haloperidol, p = 2.03. No patient developed acute dystonia compared to 6.66% of patients with haloperidol, p = 2.59. Conclusion: IM olanzapine was comparable to IM haloperidol in reduction of symptoms of acute agitation in schizophrenia during first 24 hours of treatment, the efficacy of both being evident within 2 hours after first injection. More Extra pyramidal symptoms were observed during treatment with IM haloperidol than with IM olanzapine.

Serotonin [1A] receptor agonism in the expression of behavioral dopaminergic supersensitivity in subchronic haloperidol treated rats

The idea that serotonin [5-hydroxytryptamine; 5-HT] is contributed in schizophrenia has long been advocated and alterations in 5-HT neurotransmission has been hypothesized to modulate both the therapeutic and extrapyramidal symptoms [EPS] liability of conventional neuroleptics. The 8-hydroxy-2-[di-n-propylamino] tetralin [8-OH-DPAT], a preferential 5-HT1A ligand, has been reported to attenuate EPS functions of haloperidol in animals. In view of a possible role of 5-HT1A receptors in the management of EPS functions of a neuroleptic drug, the present study was designed to investigate behavioral responses of 8-OH-DPAT at a challenge dose of 0.5mg/kg in rats with subchronic haloperidol administration at a dose of 5mg/kg twice daily for 5 days. The intensity of 5-HT syndrome provoked by 8-OH-DPAT was taken as a measure of postsynaptic responses. In the present study administration of haloperidol at a dose of 5mg/kg twice daily for 5 days decreased locomotion significantly [p<0.01] in familiar [home cage] environment. Subchronic administration of haloperidol at the same dose elicited significant [p<0.01] cataleptic responses in rats when compared with saline treated rats. Results revealed that 8-OH-DPAT-induced hyperlocomotion [p<0.05] and forepaw treading [p<0.1] were significantly smaller in rats pre-treated with haloperidol for 5 days than repeatedly saline injected rats. Conversely, the other components of the syndrome i.e. flat body posture [p<0.001], hind limb abduction [p<0.001] and straub tail [p<0.01] were significantly greater in repeated haloperidol treated rats when compared with repeated saline injected rats. These findings help to demonstrate a causal link between the upregulation of DA-D2 receptors and the decrease in the effectiveness of presynaptic 5-HT1A receptors following subchronic haloperidol administration and this may further help to yield an antipsychotic agent with an improved profile of efficacy to EPS, thereby widening its therapeutic window

Neurochemical and behavioral effects of M-CPP in a rat model of tardive dyskinesia

Present study was designed to monitor the responsiveness of 5HT [5-Hydroxytryptamine] -2C receptors following the long-term administration of haloperidol in rats. Effects of m-CPP [meta-Chlorophenyl piperazine] were monitored 48h after withdrawal from repeated [twice a day for 5 week] administration of haloperidol [at the dose of 1mg/kg]. Vacuous chewing movements [VCMs] were monitored on weekly basis. Two days after withdrawal, animals were injected with saline [1ml/kg of body weight] or m-CPP [3mr/kg of body weight]. Activities in open field and light dark activity box were monitored 15 and 30 min post injection respectively. Animals were then decapitated [4h post injection] to collect dorsal striatum [DS] samples for the neurochemical analysis by HPLC-EC [High performance Liquid Chromatography with Electrochemical detection] method. Results from the present study showed significant hypolocomotive effect of m-CPP [p<0.05] in both repeated haloperidol as well as repeated saline injected rats. Neurochemical analysis of DS by HPLC-EC method showed that administration of m-CPP significantly [p<0.05] decreased 5-HIAA [5-Hydroxyindol acetic acid] in repeated haloperidol injected rats. In conclusion, present study provides evidence that 5HT-2C receptors become hypersensitive in a rat model of Tardive Dyskinesia [TD]. These findings have potential implication in the treatment of TD and attenuation of EPS induced by typical neuroleptics

Atypical antipsychotics side effects, an update review

Although the novels anti psychotic's drugs are usually grouped together as a category, they are significantly different in many aspects. One is there side effect property. In there affinity to cause, EPS, and Tardive Dyskinesia - the data are still out, although, Clozapine and Quetiapine will cause less TD as compared to Risperidone and Olanzapine. The diabetes mellitus and the weight gain, is an important issue with the atypical anti-psychotics, particularly with Olanzapine and Clozapine. In Japan, the government has issued a warning stating that, Olanzapine is contraindicated in patients with pre-existing diabetes. Patients should be informed of the risk of diabetes with Olanzapine and their blood glucose should be monitored. On 05/03/02, the authorities in the UK have initiated a review of diabetes with Olanzapine because of 40 cases of diabetes four were of diabetic acidosis and one death. The QTc prolongation story, however, in some opinions, is a marketing gimmick then the actually data supports the likelihood of QTc prolongation with Ziprasidone

Análisis ultraestructural comparativo en pacientes con enfermedad de Parkinson y ratas viejas / Ultraestructural comparative analysis between Parkinson disease patients and aged rats

Los pacientes con enfermedad de Parkinson idiopático presentan pérdida neuronal de la sustancia negra parte compacta y la consecuente degeneración de la vía nigroestriatal; por otro lado, se ha reportado que los animales viejos también tienen pérdida de dicha inervación. El objetivo del presente trabajo fue comparar los cambios neurodegenerativos en el neuropilo del núcleo caudado de pacientes parkinsónicos y de animales viejos, con el fin de comparar los cambios que sufre dicho núcleo en los dos procesos degenerativos. En el análisis ultraestructural se utilizaron fragmentos del núcleo caudado de pacientes con enfermedad de Parkinson (n= 4) y de ratas viejas de 36 meses de edad (n= 4), para lo cual se midieron 100 botones presinápticos por caudado y se observó la estructura postsináptica y el número de contactos que establecía el botón con la misma estructura. Los resultados muestran que tanto los pacientes con enfermedad de Parkinson como las ratas viejas presentan un incremento estadisticamente significativo en el tamaño de los botones sinápticos, aumento en el número de contactos axodendríticos y aumento en el número de contactos dobles en comparación con los controles. Los datos indican que los pacientes parkinsónicos presentan alteraciones ultraestructurales similares a las de los animales viejos, alteraciones debidas a la ineficiente inervación dopaminérgica procedente del mesencéfalo, por lo cual se considero que el envejecimiento en animales es un buen modelo para el estudio de la neurodegeneración.

Haloperidol, biperideno e parkinsonismo / Haloperidol, biperiden and parkinsonism

O autor fez uma extensa revisäo bibliográfica sobre os neurolépticos, em especial o haloperidol, bem como sobre as reaçöes extrapiramidais, com atençäo principal ao parkinsonismo, com descriçäo de quadros e tratamentos indicados

Hematoma tegmento-mesencefálico espontâneo: aspectos neurocomportamentais do terço rostral do tronco encefálico humano / Spontaneous tegment-mesencephalic hematoma: neurobehavioral aspects of the rostral third of the human brainstem

O tegmento do mesencéfalo e área complexa, dada a quantidade de fibras que o atravessam, provenientes de circuitos locais, de sistemas ativadores e de feixes descendentes dos hemisférios cerebrais. No presente artigo, relatamos o caso de um senhor de 67 anos, que sofreu hemorragia mesencefálica de localizaçao tegmental, vindo a falecer 1 mês depois. Inicialmente, foi julgado em coma, por apresentar ptose bilateral, ausência de fala e de movimentos espontâneos. Por volta da segunda semana, descobriu-se que podia cumprir comandos verbais, sentar, sustentar-se de pé e andar. O caso demonstra o quanto o diagnóstico do coma em bases clínicas pode ser enganoso em pacientes como esse, no qual a aparente irresponsividade de olhos fechados se deve à combinaçao inesperada de abulia e oftalmoplegia.

A Case of Athetosis in Basal Ganglia Calcification Associated with Hypoparathyroidism

Extrapyramidal tract motor disorder in calcification of basal ganglia probably occurs when the deposition of acid mucopolysaccharides in the basal ganglia is severe enough to lead to neuronal loss. Basal ganglia calcification has been noted to occur with higher incidence and intensity in encephalitis lethargica, carbon monocide intoxication, anoxia, tuberous sclerosis, toxoplasmosis, hypothyroidism and hypoparathyroidism. The neurologic disorder is frequently reversible with treatment in patients with basal ganglia calcification who have hypoparathy-roidism. We report a patient with idiopathic hypoparathyroidism associated with bilateral calcification of the basal ganglia and athetoid movement. This is the first case report in Korea.

The Characteristic and Origin of Motor Evoked Potential in Rats

Motor evoked potential(MEP) produced by cortical surface or transcranial stimulation has evolved as a new clinical and experimental tool to monitor the integrity of motor pathways and to map motor cortex. Clinical assessment of motor system using MEP has further advanced with recent development of the magnetic stimulator. The primary concept using MEPs for test of motor pathways was based on the assumption that pyramidal neurons in the motor cortex are activated by electrical stimulation applied on the cerebral cortex and synchronized compound action potentials are conducted mainly along the corticospinal tracts in the spinal cord. However,recent studies indicated that the origins of the Meps in non primates may differ from those previously believed. In order to use MEPs as a clinical or experimental tool, it is essential to clarify the origin of MEPs. Therefore, goals of this study were : (1) to investigate the origin of MEPs, and (2) to design the most reliable but simple method to evoke and monitor MEPs. In a total of fifteen rats, MEPs were produced by cortex to cortex stimulation and were monitored using a pair of epidural electrodes. Using varying stimulus intensities, the amplitudes and latencies of MEPs were statistically analyzed. The latencies and amplitudes of the MEPs in these animals showed surprisingly large standard deviations, which were partially resulted in these animals showed surprisingly large standard deviations, which were partially resulted from convergence of neighboring waves during high stimulation intensities. Wave forms of MEPs were also varied greatly depending on the position of recording electordes. At low stimulus intensities, most consisten MEPs were obtained when the stimulating electrodes were placed on the hard palate and the temporal muscle, not on the motor cortex. This observation indicates that the primary source of MEPs is not the motor cortex in the rat. When the potentials generated by direct stimulation of motor cortex and those generated by reticular nuclei were monitored epidurally in the same preparation using the same electrodes, these potentials generated by different sources actually identical in their latencies and wave forms. However, the threshold stimulus intensities evoking these potentials were quite different in the two metholds. The threshold was much lower to evoke potentails by reticular nuclei stimulation. It suggests that MEPs are geneated by the reticular nuclei or brain structure located in the brain stem. The observation that the motor cortex play no major roles in generating MEPs was confirmed by sequential sections of neural axis from the motor cortex to brain stem in three rats. All these findings suggested that neither direct motor cortex stimulation not transcranial stimulation did evoke MEPs originating from the motor cortex in rat. These stimulating methods activate reticular nuclei by stimulus current spread to the brain stem. Since the reticular formation plays an important role in motor function in rats, MEP originated from reticular nucleus can be an important testing of the motor function in rats. Moreover, transcranial stimulation of the brain is technically easy. This technique producing MEPs originated from reticular nucleus can be useful to monitor the integrity of motor pathways.

The Intraspinal Pathways Conducting Motor Evoked Potentials in Rats

Recently, motor evoked potential(MEP) using cortical surface of transcranial stimulation have been used to monitor the integrity of motor pathways and map motor cortex in human and animal. The primary concept using motor evoked potentials(MEPs) for test of motor pathways was based on the assumtion that pyramidal neurons in the motor cortex are activated by electrical stimulation applied on the cerebral cortex and synchronized compound action potentials are conducted mainly along the corticospinal tracts in the spinal cord. However, the origins and the descending pathways of these MEPs in small animals may be different from those of potentials evoked by intracortical microstimulation because of current spread. Our previous study revealed that the origns of the MEPs in rats differed from those previously believed and may be reticular nuclei. To further clarify those results and localize the intraspinal pathways conduction MEPs, consecutive vertical and/or horizontal sections of the spinal cord were performed at T9 cord level in twelve rats. MEPs were recorded at T2/3 and L2/3 before and after each section and sequential alterations of MEPs were observed. In six rats, the stimulation was alternated between the right and left cortex and the lateralities of conduction pathways were compared. All six cases showed no differences of MEPs and pattern of wave abolition after each section between right and left brain stimulation. The alteration of MEPs after each consecutive section was categorized by analyzing latency shift, amplitude change, and disappearance of waves. We divided a cross section of T9 spinal cord into forty-six squares. If one of the categorized changes occurrd after cutting an area, the appropriate score was given for the area since more change of waves meant more significant contribution of the cut area to conduction of MEPs. The score of twelev rats were summed in each forty-six spots and map showing the distribution of MEPs was constructed. The map revealed that MEPs were conducted along the wide area of ventral and lateral funiculus of the spinal cord but mainly along the medial portion of the ventral funiculus of the spinal cord but mainly along the medial portion of the ventral funiculus and ventral portion of the larteral funiculus through which reticulospinal and vestibulospinal tracts pass. No conduction of MEPs along the corticospinal tracts was confirmed. This finding supports the result of our previous study. However, this extrapyramidal MEP conducted along ventral spinal cord in addition to somatosensory evoked potential(SSEP) which is conducted along posterior funiculus can be useful to monitor the integrity of the whole spinal cord. Moreover, the extrapyramidal MEP can be more useful than pyramidal MEP in rats because the reticular formation plays a more important role in motor function and pyramidal tract is located in posterior funiculus.

Prevalencia de manifestaciones extrapiramidales agudas secundarias al uso de neurolépticos en un grupo de pacientes psiquiátricos hospitalizados / Prevalence of acute extrapyramidal side effects due to neuroleptics use in a group of hospitalized psychiatric patients

Se evaluó la presencia de manifestaciones extrapiramidales agudas secundarias al uso de neurolépticos por medio de la escala de Simpson-Angus en un grupo de 112 pacientes psiquiátricos hospitalizados. La prevalencia de pseudoparkinsonismo fue de 51,7% y 30,3% según se utilice como criterio clasificatorio un punto crítico de 3 ó 6 en el instrumento de evaluación. La presencia de pseudoparkisonismo está en relación inversa con la edad. La razón hombres v/s mujeres corresponde a 1:2,77 para punto de corte en 6, siendo las diferencias estadísticamente significativas. La manifestación más frecuente corresponde a rigidez de extremidades superiores. El temblor fue un signo relativamente poco frecuente. La totalidad de efecto extrapiramidales agudos se agrupa entre un 96% a 100% entre los rangos leve a moderado. No se observan diferencias significativas en cuanto a la presencia de pseudoparkinsonismo para distintos neurolépticos, dosis promedio día y uso de antiparkinsonianos. Se observan diferencias significativas en cuanto a la presencia de pseudoparkinsonismo para pacientes con daño orgánico cerebral. Sin embargo, estos hallazgos deben interpretarse con reservas. Destacan diferencias significativas en cuanto a resistencias a desarrollar pseudoparkinsonismo, por razones poco conocidas, en pacientes con mayor número de hospitalizaciones, mayor número de días de estada y mayor tiempo de uso regular de neurolépticos, sin existir diferencias significativas en las dosis promedio día de antipsicóticos. La prevalencia de acatisia fue de 0,8%. Ningún paciente al momento del corte presentó distonía aguda. Las implicancias epidemiológica, clínica y terapéutica de los resultados son discutidas

Motor hemiplegia and the cerebral organization of movement in man: II. The myth of the human extrapyramidal system

Após revisäo sumária do conceito de sistema extrapiramidal, säo apresentadas evidências clínicas e anatômicas contra sua importância relativa no homem. Propöe-se que as estruturas tradicionalmente agrupadas sob o rótulo extrapiramidal efetuem a maior parte de suas atividades funcionais, respectivamente, por intermédio dos próprios feixes piramidais. Tais estruturas - centradas no núcleos da base dos hemisférios cerebrais, no cerebelo e, possivelmente, também, na áreas límbicas do prosencéfalo -, de acordo com nossa proposiçäo säo, na verdade pre-piramidais. Esse modelo se baseia na análise clínica de pacientes, está de acordo com mais de um século de verificaçöes anatômicas em cérebros humanos e depöe a favor da noçäo de singularidade do cérebro humano

Bases farmacológicas para o tratamento dos efeitos extrapiramidais dos antipsicóticos / Pharmacological basis for the treatment of extrapyramidal effects of antipsychotics

Os efeitos extrapiramidais dos neurolépticos säo devido a sua açäo no sistema nigro-estriatal, causando aparecimento de desordens diversas, reversíveis e irreversíveis. A mais freqüente é o pseudo-parkinsonismo, e sua origem está em um desequilíbrio acetilcolina-dopamina e é inversamente proporcional à atividade anticolinérgica do medicamento. Na discinesia tardia, ao contrário do que ocorre no pseudo-parkinsonismo, há um aumento da transmissäo dopaminérgica em conseqüência de uma supersensibilidade de desnervaçäo. O tratamento, para o pseudo-parkinsonismo é feito com anticolinérgicos. Näo há, no entanto, consenso no tratamento ideal para a discinesia tardia