Kluver-Bucy Syndrome After Minor Brain Injury

Kluver-Bucy Syndrome After Minor Brain Injury

It has been proposed that self-awareness (SA), a multifaceted phenomenon central to human consciousness, depends critically on specific brain regions, namely the insular cortex, the anterior cingulate cortex (ACC), and the medial prefrontal cortex (mPFC). The extended period of hours to weeks over which tissue damage continues to occur makes this disorder a candidate for gene therapy. Head injuries that cause a concussion, whether from a car accident or sports, can lead to confusion and problems remembering new information. There was also a decrease in the volume of the GCL and the number of GCL neurons after TBI in both FGF-2–/– and FGF-2+/+ mice, but the decrease in both was greater in FGF-2–/– mice at 35 days. A common feature of these loci is that they contain a repeated array of transcriptionally active genes encoding small structural RNAs. The case of an ascending herpetic intrauterine infection after rupture of the membranes raises the question of prevention and suppressive antiviral therapy. Moreover, they confirm the reliability of information theoretic measures for characterizing the structure of the surviving memory representations in memory-impaired patient populations.

Parallel CD137-based CD4+ T cell research showed discrete oligospecific recognition of HSV-1 antigens. Other features include (1) irresistible impulse to touch objects, (2) placidity (absence of emotional response) in which the patient becomes apathetic and indifferent to emotional stimulus with loss of facial animation (sometimes simulating affective depressive state), and (3) marked increase in sexual activity, with no concern for social appropriateness. Amnesia and aphasia are invariably neurologic symptoms of KBS in humans. She has an IQ of around 52 and has obsessive compulsivity. The activation of microglia and formation of ramified microglial clusters was first noted by Victor Babeş while studying a rabies case in 1897. You can feel at home here. Fig.1 shows sustained function in minocycline (lower panels) treated compared to untreated CNS cells following HSV infection.
Kluver-Bucy Syndrome After Minor Brain Injury

*Bleeding in the brain which can lead to brain injury. O- Other infections, including Hepatitis B, syphilis, and the virus herpes zoster, that causes chicken pox. Computed tomography is the standard method for demonstrating macroscopic brain trauma, such as contusion or hemorrhage. Tissue section coordinate, bregma –1.9 mm. Depending on the severity of the trauma, DAI may cause macroscopic or microscopic injury throughout the white matter of the cerebral hemispheres. Furthermore, binding of HSV-1 to the various subclasses of serum lipoproteins has been described, including the interaction of purified glycoprotein B from HSV-1 with ApoE (10). In this report, we have explored the protective effect achieved by the delivery of the vα22βgalα4Bcl-2 to the striatum after, rather than in anticipation of middle cerebral artery occlusion (MCAO).

Introspective SA relies on higher-order executive, attentional and metacognitive functions, which enable introspection, the ability to perform a more or less controlled reflection on one’s own mental states, behaviors, and their consequences. First, brain injury may cause focal (as in hemiparesis) or diffuse (as in dementia) neurologic impairment, but behavioral, emotional, and personality change may also be important manifestations of brain disease. Here we concentrate on the first class of hypotheses. The patient’s change in language should have initiated the need for more complete neuropsychologic testing. 9th ed. FGF-2 KO mutant mice (FGF-2–/– mice) and WT littermates (FGF-2+/+ mice) were generated from two heterozygous mating pairs (FGF-2+/–, SV129/Black Swiss background) (generously provided by Thomas Doetschman, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA) (36). This condition is due to physiologic and structural brain injury related to DAI.

Clinicians now have the opportunity to demonstrate the anatomy and pathology of DAI using MRI and perhaps in the future will be able to learn about physiologic and biochemical substrates of DAI by using functional MRI, single photon emission CT, positron emission tomography, and MR spectroscopy. This case indicates how even mild trauma to the brain can cause significant neurologic and behavioral disorders. Since KBS has most commonly been associated with severe brain injury, the clinical outcome has usually been poor. The case described herein shows that this is not invariably true. Although CT is an excellent imaging modality for severe traumatic injuries necessitating emergency intervention, in those patients who have neurobehavioral disturbances after mild brain trauma, we must move beyond CT and use MRI to search for structural brain lesions. This case has important implications for all physicians who treat patients with traumatic brain injury.

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