Unilateral caudate infarct following pituitary adenoma resection.

Cerebral ischemic complications after pituitary surgery are not frequently reported. Multiple mechanisms have been proposed, including vasospasm, and delayed cerebral ischemia resulting from postoperative subarachnoid bleeding. Given the unknown etiology of vasospasm following these situations, little is known about its prevention. Through a case report and bibliographic review, the authors warn about the importance of recognizing key signs postoperatively that could indicate increased risk for cerebral vasospasm and must be recognized in a timely manner, with appropriate treatment strategies implemented once these symptoms present.

Endocannabinoid neuromodulation in the neostriatum decreases the GABAergic striato-nigral disinhibitory function and increases the nigro-collicular inhibitory pathway activity.

We previously reported the involvement of neostriato-nigral projections in the organisation of innate fear and panic attack-like responses organised by dorsal midbrain neurons, such as the periaqueductal grey matter and the deep layers of the superior colliculus (dlSC). In addition, several lines of evidence have demonstrated that cannabinoid receptor type 1 is found in the neostriatum (caudate nucleus and putamen; CPu). In the present study, we investigated the role of endocannabinoid neuromodulation in CPu in the expression of unconditioned fear-related behavioural responses elicited by microinjections of the γ-aminobutyric acid (GABA)A receptor selective antagonist bicuculline (BIC) in the dlSC. Wistar rats received injection of vehicle or anandamide (AEA) at 0.5, 5, 50, 100 pmol in CPu, followed by injections of BIC in a dose of 40 ng in the dlSC. The treatment of the CPu with AEA in a dose of 5 and 50 pmol attenuated the unconditioned fear-related behaviour, such as defensive alertness, defensive immobility and escape, induced by GABAA receptor blockade in dlSC. These findings suggest that endogenous cannabinoids acting on CPu neurons exert an indirect modulatory influence on the activity of superior colliculus neurons, possibly through an inhibitory activity on neostriato-nigral disinhibitory connections that modulate the nigro-collicular inhibitory GABAergic pathways.

Digging deeper in the proteome of different regions from schizophrenia brains.

Schizophrenia is a psychiatric disorder that affects 21 million people worldwide. Despite several studies having been shown that some brain regions may play a critical role in the pathophysiology of schizophrenia, the molecular basis to explain this diversity is still lacking. The cerebellum (CER), caudate nucleus (CAU), and posterior cingulate cortex (PCC) are areas associated with negative and cognitive symptoms in schizophrenia. In this study, we performed shotgun proteomics of the aforementioned brain regions, collected postmortem from patients with schizophrenia and compared with the mentally healthy group. In addition, we performed a proteomic analysis of nuclear and mitochondrial fractions of these same regions. Our results presented 106, 727 and 135 differentially regulated proteins in the CAU, PCC, and CER, respectively. Pathway enrichment analysis revealed dysfunctions associated with synaptic processes in the CAU, transport in the CER, and in energy metabolism in the PCC. In all brain areas, we found that proteins related to oligodendrocytes and the metabolic processes were dysregulated in schizophrenia. SIGNIFICANCE: Schizophrenia is a complex and heterogeneous psychiatric disorder. Despite much research having been done to increase the knowledge about the role of each region in the pathophysiology of this disorder, the molecular mechanisms underlying it are still lacking. We performed shotgun proteomics in the postmortem cerebellum (CER), caudate nucleus (CAU) and posterior cingulate cortex (PCC) from patients with schizophrenia and compared with healthy controls. Our findings suggest that each aforementioned region presents dysregulations in specific molecular pathways, such as energy metabolism in the PCC, transport in the CER, and synaptic process in the CAU. Additionally, these areas presented dysfunctions in oligodendrocytes and metabolic processes. Our results may highlight future directions for the development of novel clinical approaches for specific therapeutic targets.

Ultrastructural Changes of Caudate Nucleus in Mice Chronically Treated with Manganese.

Manganese (Mn) is able to cross the blood-brain barrier and induces functional and structural alterations during the intoxication by this metal. Therefore, the effects of chronic administration of Mn in the caudate nucleus of mice were evaluated by electron microscopy. Male albino mice were injected intraperitoneally with MnCl2 (5 mg/kg/d) 5 d per week during 9 weeks. The control group received only 0.9% of NaCl solution. The caudate nuclei were extracted and subsequently processed to be observed on a conventional transmission electron microscope at 2, 4, 6, and 9 weeks after treatment. A high percentage of vacuolated and swollen mitochondria were found throughout all the analyzed periods. Myelin disarrangement and ultrastructural alterations related to edema were observed increased in Mn-treated mice at week 9. Granular degeneration of myelin at week 9 accompanied with deposition of electron dense granules in the neuropil was also observed. Edema in neuropil and glial cells was detected from week 2 to week 9 accompanied by swollen mitochondria. Neuronal bodies, synaptic terminals, and perivascular cells were found swollen. Decreased electron density in postsynaptic areas and decreased and dispersed synaptic vesicles in presynaptic areas were noted in Mn-treated animals. Some neurons from Mn-treated mice showed cisternae dilation of the Golgi apparatus. These results suggest that Mn-treatment produces structural alterations in the caudate nucleus that could be responsible for some of the neurotoxic effects of this metal.

Language impairment in Huntington's disease / Alterações de linguagem na doença de Huntington

Language alterations in Huntington's disease (HD) are reported, but their nature and correlation with other cognitive impairments are still under investigation. This study aimed to characterize the language disturbances in HD and to correlate them to motor and cognitive aspects of the disease. We studied 23 HD patients and 23 controls, matched for age and schooling, using the Boston Diagnostic Aphasia Examination, Boston Naming Test, the Token Test, Animal fluency, Action fluency, FAS-COWA, the Symbol Digit Modalities Test, the Stroop Test and the Hooper Visual Organization Test (HVOT). HD patients performed poorer in verbal fluency (p<0.0001), oral comprehension (p<0.0001), repetition (p<0.0001), oral agility (p<0.0001), reading comprehension (p=0.034) and narrative writing (p<0.0001). There was a moderate correlation between the Expressive Component and Language Competency Indexes and the HVOT (r=0.519, p=0.011 and r=0.450, p=0.031, respectively). Language alterations in HD seem to reflect a derangement in both frontostriatal and frontotemporal regions.

Alterações de linguagem são descritas na doença de Huntington (DH), mas sua natureza exata e a correlação com outras funções cognitivas ainda estão em investigação. Os objetivos deste estudo foram caracterizar o prejuízo de linguagem na DH e correlacioná-lo aos aspectos motores e cognitivos da doença. Foram estudados 23 pacientes com DH e 23 controles, equiparados quanto à idade e escolaridade. Usamos os testes de Boston para Diagnóstico da Afasia, de Nomeação de Boston, Token, Modalidades de Símbolos e Dígitos, Stroop, Organização Visual de Hooper (TOVH), fluência de animais, fonêmica e verbos. Pacientes com DH apresentaram pior desempenho na fluência verbal (p<0,0001), compreensão oral (p<0,0001), repetição (p<0,0001), agilidade oral (p<0,0001), compreensão de leitura (p=0,034) e narrativa escrita (p<0,0001). Houve correlação moderada entre os índices Componente de Expressão e Competência de Linguagem e o TOVH (r=0,519, p=0,011 e r=0,450, p=0,031, respectivamente). Alterações de linguagem na DH parecem refletir prejuízos nas regiões frontostriatais e frontotemporais.