Double dissociation of the anterior and posterior dorsomedial caudate-putamen in the acquisition and expression of associative learning with the nicotine stimulus.

Tobacco use is the leading cause of preventable deaths worldwide. This habit is not only debilitating to individual users but also to those around them (second-hand smoking). Nicotine is the main addictive component of tobacco products and is a moderate stimulant and a mild reinforcer. Importantly, besides its unconditional effects, nicotine also has conditioned stimulus effects that may contribute to the tenacity of the smoking habit. Because the neurobiological substrates underlying these processes are virtually unexplored, the present study investigated the functional involvement of the dorsomedial caudate putamen (dmCPu) in learning processes with nicotine as an interoceptive stimulus. Rats were trained using the discriminated goal-tracking task where nicotine injections (0.4 mg/kg; SC), on some days, were paired with intermittent (36 per session) sucrose deliveries; sucrose was not available on interspersed saline days. Pre-training excitotoxic or post-training transient lesions of anterior or posterior dmCPu were used to elucidate the role of these areas in acquisition or expression of associative learning with nicotine stimulus. Pre-training lesion of p-dmCPu inhibited acquisition while post-training lesions of p-dmCPu attenuated the expression of associative learning with the nicotine stimulus. On the other hand, post-training lesions of a-dmCPu evoked nicotine-like responding following saline treatment indicating the role of this area in disinhibition of learned motor behaviors. These results, for the first time, show functionally distinct involvement of a- and p-dmCPu in various stages of associative learning using nicotine stimulus and provide an initial account of neural plasticity underlying these learning processes.

The role of the ventrolateral caudoputamen in predatory hunting.

The ventrolateral caudoputamen (VLCP) is well known to participate in the control of orofacial movements and forepaw usage accompanying feeding behavior. Previous studies from our laboratory have shown that insect hunting is associated with a distinct Fos up-regulation in the VLCP at intermediate rostro-caudal levels. Moreover, using the reversible blockade with lidocaine, we have previously suggested that the VLCP implements the stereotyped actions seen during prey capture and handling, and may influence the motivational drive to start attacking the roaches, as well. However, considering that (1) lidocaine suppresses action potentials not only in neurons, but also in fibers-of-passage, rendering the observed behavioral effect not specific to the ventrolateral caudoputamen; (2) the short lidocaine-induced inactivation period had left a relatively narrow window to observe the behavioral changes; and (3) that the restriction stress to inject the drug could have also disturbed hunting behavior, in the present study, we have examined the role of the VLCP in predatory hunting by placing bilateral NMDA lesions three weeks previous to the behavior testing. We were able to confirm that the VLCP serves to implement the stereotyped sequence of actions seen during prey capture and handling, but the study did not confirm its role in influencing the motivational drive to hunt. Together with other studies from our group, the present work serves as an important piece of information that helps to reveal the neural systems underlying predatory hunting.

Analysis of five cases with neurogenic stuttering following brain injury in the basal ganglia.

UNLABELLED: This study examined stuttering patterns in five patients with basal ganglia injury. None of the patients had a history of developmental stuttering. Four patients were right-handed; one patient was ambidextrous. Stuttering tests administered to patients assessed sentence repetition, reading aloud, explanations of a comic strip, and conversation. Accessory behaviors such as facial grimaces, associated movements of the limbs, and avoidance behaviors were observed. The results of this study differ from those of previous studies of neurogenic stuttering in several respects: (1) blocks were frequently observed. (2) Adaptation was observed. (3) Almost all stuttering occurred at the initiation of words. (4) Across patients, stuttering frequency did not vary in a consistent manner with speaking task. New speech characteristics for neurogenic stuttering without aphasia following injury to the basal ganglia are described. EDUCATIONAL OBJECTIVES: After reading this text, the reader will be able to: (1) provide characteristics of neurogenic stuttering after the basal ganglia in patients without aphasia; (2) discuss the difference of the features and characteristics of stuttering between previously reported patients and present patients.

Amaurosis y necrosis bilateral del putamen en la intoxicación por metanol. Probable disfunción mitocondrial de origen tóxico / Bilateral blindness and putamen necrosis in methanol poisoning. Probable toxic induced mitochondrial dysfunction

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Monocyte chemoattractant protein-1 correlates with subcortical brain injury in HIV infection.

Various biomarkers have been suggested as associative or predictive of HIV-associated neurocognitive impairment. Plasma levels of monocyte chemoattractant protein 1 (MCP-1), tumor necrosis factor alpha (TNF-alpha), and hematocrit were evaluated for relationships with diffusion tensor imaging measurements of centrum semiovale, caudate, and putamen. MCP-1 levels correlated with tissue status (mean diffusivity) in all examined regions. Plasma markers were also significantly correlated with anisotropy measurements in centrum semiovale (TNF-alpha) and putamen (hematocrit).

The effect of the destruction of the caudate-putamen on the development of amygdaloid kindling and kindled seizures.

To elucidate the possible roles of the caudate-putamen (CP) on the development of amygdala (AM) kindling and AM-kindled seizures, the bilateral CP were destroyed by intra-CP injection of ibotenic acid (0.5 or 1.0 microg per side) before the AM kindling or after completion of the AM kindling. Prior destruction of the CP, especially by 0.5 microg ibotenic acid injection, caused a significant delay in seizure development. However, after completion of the AM kindling, bilateral destruction of the CP significantly suppressed AM-kindled seizures in proportion to lesion size, however, all animals reached a stage 5 seizure by additional stimulations and established AM kindling. These findings suggest that the intact CP modulates the development of the AM kindling and the generalization and/or expression of the kindled AM seizures, and that the CP plays an important role in the generalization and/or expression of the kindled AM seizures.

Region-specific attenuation of a trypsin-like protease in substantia nigra following dopaminergic neurotoxicity by 1-methyl-4-phenyl-1,2, 3,6-tetrahydropyridine.

We analysed apoptosis, caspase-1 and -3, and trypsin-like protease activity in the nigrostriatal pathway during 1-methyl-4-phenyl-1,2,3, 6-tetrahydropyridine (MPTP)-induced neurotoxicity. MPTP injected (30 mg/kg, i.p., twice, 16 h apart) mice were sacrificed on 1, 2 and 7 days. DNA extracted from nucleus caudatus putamen (NCP) and substantia nigra (SN) was subjected to agarose gel electrophoresis. Typical apoptotic-like DNA cleavage was absent in SN or NCP after this dose of MPTP. A trypsin-like protease activity was significantly decreased in SN and not in NCP. While caspase-3 activity in the whole brain was increased significantly, caspase-1 activity was unaffected. Striatal dopamine content was decreased to 75% by 7 days. The absence of typical DNA 'ladder' when there was severe striatal dopamine depletion suggests that in vivo MPTP-mediated dopaminergic neurotoxicity may not involve apoptotic cell death, and explains why in mice MPTP-induced dopamine depletion is transient. The region-specific decrease in trypsin-like protease activity and absence of caspase-3 activation in SN signify the importance of trypsin-like protease in the regulation of apoptosis in MPTP-neurotoxicity in mice.

In vivo PET studies of the dopamine D2 receptors in rhesus monkeys with long-term MPTP-induced parkinsonism.

Studies of dopamine (DA) receptor binding in early parkinsonian patients, or in models of Parkinson's disease, have revealed a supersensitivity of the D2-like receptor subtype as compared to age-matched controls. The lack of upregulation in advanced patients is often attributed to the effects of prolonged antiparkinsonian therapy, but the impact of therapy vs. intrinsic mechanisms in untreated patients or animals with long-term lesions of the DA nigrostriatal pathway has been difficult to address. We studied, in vivo, by PET using the DA D2 receptor ligand raclopride, the status of the DA receptors in normal rhesus monkeys and those with acute (3 months) or long-term (10 years) MPTP-induced nigrostriatal lesions. Compared to age-matched controls, there was no change in raclopride binding in MPTP-treated animals without parkinsonian symptoms. There was a significant increase in raclopride binding in the putamen (but not caudate nucleus) of all the animals displaying rigidity, hypo- and bradykinesia. This increase was greater in the animals with acute lesions (32%) than with established, long-term lesions (18%). There was no correlation between the postmortem striatal DA concentrations and in vivo raclopride binding but there was a correlation between PET raclopride binding and [(3)H]raclopride binding in vitro. Complex changes in D2 receptor binding occur in various stages of parkinsonism. Antiparkinsonian therapy is unlikely to be solely responsible for the lack of upregulation found in advanced parkinsonian patients but may be a contributing factor.

Is the spatial distribution of brain lesions associated with closed-head injury predictive of subsequent development of attention-deficit/hyperactivity disorder? Analysis with brain-image database.

PURPOSE: To determine whether there is an association between the spatial distribution of lesions detected at magnetic resonance (MR) imaging of the brain in children after closed-head injury and the development of secondary attention-deficit/hyperactivity disorder (ADHD). MATERIALS AND METHODS: Data obtained from 76 children without prior history of ADHD were analyzed. MR images were obtained 3 months after closed-head injury. After manual delineation of lesions, images were registered to the Talairach coordinate system. For each subject, registered images and secondary ADHD status were integrated into a brain-image database, which contains depiction (visualization) and statistical analysis software. Using this database, we assessed visually the spatial distributions of lesions and performed statistical analysis of image and clinical variables. RESULTS: Of the 76 children, 15 developed secondary ADHD. Depiction of the data suggested that children who developed secondary ADHD had more lesions in the right putamen than children who did not develop secondary ADHD; this impression was confirmed statistically. After Bonferroni correction, we could not demonstrate significant differences between secondary ADHD status and lesion burdens for the right caudate nucleus or the right globus pallidus. CONCLUSION: Closed-head injury-induced lesions in the right putamen in children are associated with subsequent development of secondary ADHD. Depiction software is useful in guiding statistical analysis of image data.

Fisioterapia em acidente vascular hemorragico putaminal direito: estudo de caso / Physical therapy approuch in right putaminal hemorrhagic stroke: case report

O objetivo do estudo foi caracterizar o quadro funcional de um paciente com diagnostico de acidente vascular cerebral hemorragico putaminal e verificar os efeitos da intervencao fisioterapica, utilizando os procedimentos da facilitacao neuromuscular proprioceptiva. Empregou-se o delineamento de sujeito unico, observando...

[Computed tomography in methanol intoxication]. / Tomografia computadorizada na intoxicação por metanol. Relato de caso.

We had the opportunity to follow a methanol intoxication case with CT scans, at the 1st and 6th day after admission. Symmetrical putaminal and white matter lesions were seen on the last CT examination, and occurred with the worsening of neurological manifestations, despite the appropriated treatment. The CT demonstration of brains lesions disclosed the toxic effect of the methanol and could be a guideline to the neurological prognosis.

Tomografia computadorizada na intoxicaçäo por metanol: relato de caso / Computed tomography in methanol intoxication

Tivemos a oportunidade de acompanhar com exames de TC caso de intoxicaçäo por metanol. O paciente foi submetido ao exame no momento da internaçäo e após seis dias, pela persistência de quadro neurológico grave. Observou-se nesta última a presença de lesöes putaminais simétricas e da substância branca subcortical, apesar do tratamento adequado. A comprovaçäo tomográfica de lesöes cerebrais evidenciou efeito tóxico do metanol e pode orientar o prognóstico neurológico

Posttraumatic paroxysmal nocturnal hemidystonia.

The term "nocturnal paroxysmal dystonia" has been used to describe patients who display paroxysmal episodes of dystonic-dyskinetic movements arising during nonrapid eye movement sleep, in particular stages 2-3 (Lugaresi E, Cirignotta F. Hypnogenic paroxysmal dystonia: epileptic seizure or a new syndrome. Sleep 1981;4: 129-138). The pathogenesis of these attacks has remained controversial. We describe a patient with posttraumatic paroxysmal nocturnal hemidystonia. Acetazolamide led to improvement.