Neurological Disorders

Historically, defining consciousness has been exceedingly difficult and perplexing to neurologists and neuroscientists. Studying consciousness objectively in the human brain has been exponentially problematic. However, as newer technological approaches evolve and more is understood about the complexities of the human brain, novel ways of objectively understanding human consciousness have emerged. In this paper I briefly review two new methods of defining consciousness with the novel EPIC consciousness paradigm and the neurogenetic model; as well as two new neurophysiological discoveries that change the way human consciousness is objectified. Collectively, these breakthroughs may enable investigators to better understand both human consciousness and disorders of consciousness.

This paper is a deep and fortunate revision of medical literature about causes of schizophrenia and some future treatment of this controversial disease. The author carries the lector to the concept of neuroplasticity, the roll of Dopamine and GABA, as well as the excitatory glutamate over the dorsolateral prefrontal cortex of the brain, where he sustains (with important literature) reside the crucial anatomo-phisiological part of the brain for schizophrenia. Very interesting aspects are explained, based on studies performed since 2000 by Elvevag [1], over presented brain atrophy in schizophrenia due to neurotoxicity and neurodegeneration “that involved loss of neurons in the gray matter with marked reduction in the number and size of dendritic extensions”. The author tries to explain after Wakade´s [2] investigations that haloperidol produces neurotoxicity and cell apoptosis opposite to second generation antipsychotics that stimulate neurogenesis.

Background: Statistics is a powerfull tool in the hands of an expert but in the hands of a fool it can result in devastating conclusions, since it can fool the whole scientific world.

Method: A simulation of 340 patients with growth hormone overexpression and visual disturbance is compared with a control group of normal expressing growth hormone in healthy individuals. Different statistical analyses have been performed.

Results: All statistical analyses performed here, show a highly significant correlation of growth hormone overexpression and visual disturbance.

Conclusion: Statistically it seems that growth hormone is a cause of visual disturbance. We know that growth hormone by itself is not causing blindness but the disease hidden behind this overexpression, namely macro adenomas does. Would we not be aware of the causative disease we would easily come to the conclusion that growth hormone is strongly associated with visual disturbance. If the knowledge about a pathologic entity is incomplete a statistical analysis alone can mislead the scientific world to very strange conclusions.

Auditory hallucinations are one of the most frequent and reliable symptoms of psychosis. However, the neurocognitive and neurophysiological bases of auditory and verbal hallucinations remain obscure. These hallucinations are thought to result from disordered monitoring of inner speech. In this article, the synaptic and psychopathological mechanisms for the auditory hallucinations are discussed. Auditory hallucinations might be occurred due to a failure of synaptic connectivity. The disturbances of the spine are caused by temporary abnormal neuronal excitations and failure of synaptic connectivity will be observed. The abnormality in the neurotransmission of glutamic acid and GABA will cause a musical hallucinations, heightened auditory awareness and “Les eidolies hallucinosiques” (which are hallucinations without delusions). By adding the abnormal neurotransmission of dopamine and /or serotonin to GABA and glutamate abnormalities, the delusions will be applied to the “Les eidolies hallucinosiques” and it will become paranoid hallucinations (“Les hallucinations délirantes”). The valproic acid that inhibits the GABA degrading enzyme and agonist of the NMDA receptor will be the first choice for “Les eidolies hallucinosiques” from immediately after onset. If the patient complains the paranoid symptoms, the dopamine and serotonin receptor antagonist will be desirable.

Background: Hurst disease is the rarest yet the most fatal form of acute demyelinating encephalomyelitis. There around 100 cases around the world, 10 of them are pediatric patients. The disease is quite severe in course and aggressive therapy is crucial to help improving the outcome. We are reporting a rather successful story of early recognition and treatment of young toddler with using all lines of known therapies simultaneously and aggressively. Case report: We are reporting 2 ½ years old girl who was previously healthy. She has some viral prodromal illness ended by severe encephalopathy. She has found to have novel H1N1 infection. Early plasma exchange and therapeutic hypothermia have been simultaneously utilized. There was obvious significant fast improvement in clinical status thereafter. Discussion: Immune therapy is advised in treating Hurst disease. One trial of hypothermia has been suggested in one case report. However, Combination of early use of plasma exchange and therapeutic hypothermia has not been reported in literature up to our knowledge. Our patient showed impressive clinical progress following these rarely used procedures. Conclusion: Recognition of autoimmune encephalitis especially the most severe forms is a must. If the patient shows enough clinical and radiological signs suggestive of Hurst disease, then aggressive immunotherapy and therapeutic hypothermia should be considered. A more favorable outcome might be reached using these therapies simultaneously

Neuroplasticity is pointed to the ability of the brain to change its molecular and structural characteristics that hinder its function. The main pathophysiological alteration in schizophrenic patients is the occurrence of a major deficit in cognitive process that is under the control of the circuitry of the dorsolateral prefrontal cortex (DLPFC) [1,2]. Additionally, this cognitive deficit in schizophrenia is partially related to the marked decrease in dopamine [DA] input to the DLPFC. However and fortunately, a compensatory response in the form of up-regulation of D1 receptor in this area of brain results in a great improvement of memory-related DLPFC activity.

Guillain Barre Syndrome (GBS) is an autoimmune inflammatory neuropathy. It affects all age group of both sexes and can lead to morbidity if untreated. It is usually preceded by an infection and has a fast progression. There are two treatment modalities practiced primarily, plasmapheresis and intravenous immunoglobulin therapy. Matrix metalloproteinases have been indicated to play a role in pathogenesis of GBS by mediating inflammation and disrupting blood nerve barrier. Greater focus needs to be put on these MMP’s as marker enzymes for early detection and/or diagnosis and as targets for therapy.

Background: Purine-rich diets and improper metabolism of uric acid result in deposition of monosodium urate crystals in multiple organs throughout the body. Gout is typically characterized by recurrent attacks of inflammatory arthritis; however, deposition of uric acid crystals in the spinal canal may result in debilitating back pain, neural compression, and progressive myelopathy. While extradural gout is a widely reported source of spinal cord compression, we present a novel case of an individual with intradural tophaceous gout in the cranial and spinal cavities. Case history: A 61-year-old African-American male presented with diplopia, masticatory difficulty, and facial pain. Serial imaging revealed an enlarging, heterogeneously enhancing mass in the left cavernous sinus with extension into the superior orbital fissure and foramen ovale, raising suspicion for a meningioma. Successful surgical resection of the cavernous lesion was undertaken to eliminate the risk of permanent ophthalmoplegia and blindness. The pathological findings were felt to be compatible with chondroma. Nine years later, after stable yearly imaging follow-up of the cranial lesion, the patient presented with progressive myelopathy. Imaging of the spine revealed enhancing, intradural lesions suggestive of calcified meningiomas. Surgical resection was undertaken to preserve motor function. Histopathologic diagnosis after spinal decompression was tophaceous gout. Retrospective review of the cranial pathology indicated that this lesion, too, was consistent with tophaceous gout. Conclusion: The pathophysiology of spinal tophaceous gout is well known and extradural lesions are not uncommon. However, multifocal intradural tophi involving intracranial and intraspinal compartments have not been previously reported. This case represents the first reported case of both intracranial and intraspinal intradural tophaceous gout causing neurological deficits.

The finding determines the dependence of body processes on STP and MCT, six processes which occur in the isolated rabbit ileum were used to prove the statement of Boy’o Universal Theory of therapy 1(BUTT 1), mainly effects of extract and Autonomic drugs on isolated rabbit ileum together with novel mathematical principles were used to show that seven normal processes (motility, secretion, metabolism, circulation, immunoreactivity, absorption, digestion) of the isolated rabbit ileum are directly proportional to activated STP and MCT and inversely proportional to inactivated STP and MCT given as Rs i i s s y y R N and thus R K N N N α = Acknowledge that from the above relation, STP magnitude responses Rsm was used base on the assumption that all body processes are responses of STP and MCT, in other words, body processes are manifestation of STP response, thus First and foremost, I posit that any number of response (Rsn) or magnitude of response (Rsm) is a function of or proportional to activated STP backbones (Ni) and inversely proportional to inactivated STP backbone (Ny). i.e. i i s s y y R N and thus R K N N N α = 1() K is a universal constant of proportionality of therapy. To estimate (Ni) for each receptor in the isolated rabbit ileum, I determined number of molecules (N) for each drug and extract and number of molecules (Nx) towards the receptor direction, also using a biomarker (isolated rabbit ileum) the magnitude of effect (contraction and relaxation) of extract/drugs on the ileum was determined by combination interactions, novel mathematical equations and quantum physics concepts, which gave me insight about the autonomic nature of the extract. Again from the combination interaction of antagonists and agonists with the extract as well as novel mathematical equation and calculation, I deduced the receptor types which combined with the extract, the couple receptor types, and the linked cascades in unlimited sense of their complexity. Again, in spite that past finding have unraveled various receptor types, limitations of characterization and crystallography abounds and so warrant use of mathematic to gain useful insight, interestingly, observed height, STP components’ flux time and mathematically determined magnitude of response (Rsm) shows strong correlation, of course as found in other findings, we assumed that alternating responses seen was due to bimodal on or off switches peculiar to STPs and MCT, these act in turn to activate many targets and therefore more than two responses might have occurred as predicted from various novel equation and calculation. The seven processes investigated are; directly; motility, indirectly; secretion, epithelial protein synthesis and transluminal absorption, digestion, circulation, and immunoreactive processes respectively, as a matter of veracity, it important to state that only the result of isolated rabbit ileum motility was obtained from which other processes were inferred, from perspective of STP and MCT vital cascade components, using platform of mathematics, in so far as this remain the case, the principle of hypothesis was investigated and lead to the emergence of Boy’o Universal Theory of Therapy (BUTT) 1, Theory 1 of BUTT called dependence theory, states that, any process; pathologic, physiologic, biochemical, genetic, metabolic and congenital occurring in the body, including drug efficacy and drawback, is directly proportional to activated signal transduction pathways (STPs) and inversely proportional to inactivated ones provided that MCT remains constant. The result was subject to both statistical analysis and mathematical calculation, for the statistical result standard deviation was 1.05 and magnitude of response (Rsm) was 27.996 at number of active components (Nc1) of 0.7 to indicate inactivation of STPs, other values show STPs activation, a fact that is of clinical, pharmacological, and biomedical importance.

Objective and importance: Symptomatic metastases to the pituitary gland are rare and often herald advanced systemic malignant disease. Distinguishing them from benign pituitary adenomas is challenging. The clinicoradiological features of three patients with pituitary metastases are presented. We also review the literature from 1970 to 2015 to formulate a diagnostic strategy. Clinical presentation: All patients were elderly with ages ranging from 65 to 82 years old. One had a previously undiagnosed prostatic carcinoma and two had known histories of primary gastric or parotid salivary gland carcinoma. Rapid visual deterioration was the most common symptom followed by ophthalmoplegia. Cranial diabetes insipidus (CDI) was observed after administrating hydrocortisone replacement in one patient. All patients had evidence of a solitary pituitary tumor on magnetic resonance imaging (MRI) of which two had discernible posterior pituitary signal changes. Trans-sphenoidal excision was performed for all patients with no procedure related complications. Two patients had visual improvement, but due to advanced systemic disease all succumbed within two months. A literature review of 475 pituitary metastases revealed that breast (37.1%) and bronchogenic carcinomas (22.1%) were the most frequently encountered primary malignancies. Among 290 symptomatic patients (22.1%) were the most frequently encountered primary malignancies. Among 290 symptomatic patients the commonest presentation was CDI (19.9%) and 12.1% had ophthalmoplegia. Of the 166 tumors with documented neuroimaging features, 31.3% had evidence of pituitary stalk thickening or enhancement followed by cavernous sinus invasion (30.1%) or was dumbbell shaped (27.7%). Conclusion: Diagnosing metastatic pituitary tumors is important for the treating clinician in order to avoid unnecessary surgical excision in patients with limited life expectancy. Patients older than 60 years, or with a history of cancer, presenting with CDI or ophthalmoplegia are red flag clinical features. For these patients we recommend investigations for occult primary malignancy when early posterior pituitary involvement orcavernous sinus invasion is demonstrated on MRI.

Background: Consensus guidelines to assist practitioners regarding patient selection for thrombectomy in acute ischemic stroke are absent. The purpose of this study is to use the Nationwide Inpatient Sample Database to evaluate the differences in patient outcomes between high-volume stroke centers that are more aggressive with using thrombectomy than those high-volume stroke center that are less aggressive. Methods: High volume stroke centers were identified for the years 2009, 2010 and 2011 in the Nationwide Inpatient Sample Database based upon having treated at least 5 patient with thrombectomy, 20 with thrombolysis, and 300 total stroke patients. Hospitals were then categorized based on the ratio of thrombectomies/thrombolyses performed each year (T/T ratio). Outcomes and mortality after thrombectomy were compared based on T/T ratio. Results: Between 2009 and 2011, 97 hospitals met inclusion criteria; there were 56,582 patients with stroke, 1,431 patients treated with thrombectomy, and 4,583 patients treated with intravenous thrombolysis at these hospitals during the study period. There were non-linear, significant associations between T/T ratio and both poor outcome (P=0.03) and mortality (P=0.01), where hospitals with the highest and lowest T/T ratios had worse outcomes and higher mortality after thrombectomy compared to moderately aggressive hospitals. Conclusion: Hospitals with moderate T/T ratios had the best clinical outcomes after thrombectomy. This data suggest the importance of both adequate treatment volumes to maintain proficiency and the use of intelligent patient selection based upon generally accepted criteria in obtaining optimal stroke outcomes after thrombectomy.

Gas embolism is a rare potentially fatal pathology and a recognized cause of cerebral ischemia and stroke [1,2]. It is a dreaded complication following invasive medical procedures, such as transthoracic needle biopsy, traumatic lung injury and decompression accidents [3-7]. Arterial gas embolism is caused by the entry of gas into the pulmonary veins or directly into the arteries of the systemic circulation [8]. Another mechanism takes place when gas enters the arterial circulation through a right-to-left cardiac or intrapulmonary shunt or if passage of bubbles through the pulmonary capillary bed occurs. Injection of 2 ml of air into cerebral circulation can be fatal [9]. Cerebral lesion can result from intracranial artery occlusion, platelet clot development on the gas-blood interface, endothelial lesion or inflammatory activation. The purpose of this study is to report an uncommon cause of stroke following an invasive medical procedure and its management.