Paraneoplastic Cerebellar Degeneration (PCD)

The disease has affected motor control over his body, but all mental functions, including cognition, have remained unaffected. His upper extremities, lower extremities, and facial muscles have been greatly compromised, thus decreasing his ability to walk, perform voluntary arm and hand movements, and produce coherent speech. Stephen has been using two canes to aid in ambulation but he has recently had trouble walking or standing without his wife’s assistance. Loss of motor control in his upper extremities has made it difficult to grasp the cane hand grips, feed himself, and perform self-care tasks, such as bathing, brushing teeth, and dressing. Stephen’s speech production has been affected causing his words to be slow, slurred, and sometimes incoherent due to decreased motor control of the tongue, mouth, and facial muscles. The disease has also affected muscles involved in swallowing, increasing his risk for choking while eating and drinking.

Such as, in the beginning, the condition attacks the site where the insult occurred and is believed to be connected to the flight or fight response of the body. CRPS can spread in the aspect that its attack migrates to other areas of the body. Generally associated with affecting the central nervous causing neuropathic pain such as burning, tingling, etc when the reality of the condition is much more widespread, CRPS affects the sympathetic and parasympathetic nervous system affecting: cognition; constitution, cardiac, and respiratory complications; systemic autonomic dysregulation; neurogenic edema; musculoskeletal changes, endocrine and dermatological manifestations; as well as affecting the urological and gastrointestinal function. More importantly, there is the potential for organ failure. Sadly, CRPS is widely misdiagnosed and misunderstood by the medical community. Moreover, due to a lack of information on the pathophysiology of CRPS and the similar absence of consistent objective diagnostic criteria, clinical trials that demonstrate effective therapies are difficult to

Mitochondrial dysfunction and oxidative stress have been consistently observed in brains of PD patients. There is increasing pharmacological and genetic evidence sustain a link between PD and mitochondrial respiratory chain dysfunction, particular a deficit in mitochondrial complex I (Franco-Iborra et al., 2015). Accidental exposure to 1-methyl-4-phenyl-1,2,3,4-tetrahydropyridine (MPTP), an mitochondrial complex I inhibitor, has been known to result in acute and irreversible syndrome that was almost indistinguishable from PD (Calne and Langston, 1983; Langston and Ballard, 1983). Later on, mitochondrial complex I inhibition has been identified in the brains of sporadic PD patients (Schapira et al., 1990). In addition, chronic systemic inhibition of mitochondrial complex I by pesticide rotenone has been found to link to sporadic PD (Betarbet et al., 2000). Interestingly, mitochondrial complex I deficiency has been found not only in the postmortem substantia nigra but also in cerebral cortex (Schapira et al., 1990), which is consistent to the cortical glucose hypometabolism observed in PD patients. Indeed, the pathology of PD has been found to involve several brain regions other than the SNc and many neurotransmitters other than dopamine (Lang and Obeso, 2004a, b). PD models using MPTP and rotenone have now been used extensively in PD research (Beal,

Cerebrum malignancy: Cancer of the focal data preparing focal point of the body. Tumors in the mind can be dangerous or considerate, and can happen at any age. Just dangerous tumors are destructive. Essential mind tumors disease at first structures in the cerebrum tissue.

Dr. Janniger, a Pediatrician at Rutgers New Jersey Medical School asserts that elevated AFP is the most constant marker for Ataxia-Telangiectasia (2007). Normally, AFP is a fetal protein made in a fetus’s liver and should drop off near or within a year of birth (Blaese, Stiehm, Bonilla, & Younger, 2013). This AFP level is elevated in 95% of patients with AT, after age 18-24 months (Blaese et al., 2013). Additionally, an MRI (magnetic resonance imaging) of the cerebellum or chest would be indicative of AT by about the age of 10; cerebral white matter demyelination and microhemorrhages would be evident (Janniger, 2017). The cerebellum would have also lost much of its volume (Chun & Gatti, 2004). Tavani describes the MRI of 19 patients on AT and correlate the appearance of these scans with the degree of neurologic deficit, the timing of which can be crucial in determining life expectancy or if an alternative diagnosis is needed (Tavani, Zimmerman, Berry, Sullivan, Gatti, &Binghmam, 2003). The team found there was a noted progression of cerebellar atrophy from the lateral areas to the superior areas over time (Tavani et al., 2003). Other laboratory findings, in addition to elevated AFP and diagnostic MRI scans, include immunological deficiencies such as low T cell levels, low IgA, IgE, and IgG, chromosomal aberrations, sensitivity to radiation, defects of cell cycle checkpoints,

central nervous system disorders such as cerebral palsy and spinal cord injury (spina bifida); motor neuron disorders such as spinal muscular atrophy; peripheral nerve disorders such as Charcot-Marie-Tooth disease; neuromuscular junction disorders such as congenital myasthenia gravis; and muscle fiber disorders such as Duchenne's muscular dystrophy currently have no known definitive treatments or cures (p. 163).

The purpose of this project was for the interns to have a greater understanding of what kind of disabilities that they will be working with, not only at Adaptive, but also as a future physical therapist. For me personally, I have never heard of cerebellar ataxia before, and it was interesting to learn how the cerebrum works, and it vital role in movement. The idea for doing this project came from our instructor Jeff Krug. At the very start of the internship, he assigned all the interns a specific disability that we had to research and do a powerpoint on. Initially we were suppose to present them, but time did not allow this. Hopefully though, he will be able to use some of the information that I have presented for future interns, or even a

(MS) is a chronic inflammatory, demyelinating, autoimmune neurodegenerative disease characterized by the disruption of the blood brain barrier (BBB), perivascular inflammation, axonal and oligodendrocyte injury, and breakdown of the myelin sheath present in the central nervous system (CNS). The Loss of myelin leads to progressive axonal damage and eventually neuronal death, resulting in neurodegeneration and functional disability in different regions in the brain and the spinal cord. According to the domain which is compromised, it could cause various symptoms such as motor dysfunction, sensory distortion, visual impairment, dyscoordination, fatigue, bladder dysfunction, cognitive impairment and depression (Goldenberg et al.,2012), and is characterized With remissions and recurring exacerbations of the disease.

Alzheimer’s is a progressive and deteriorating condition that affects the brain`s nerve cells, resulting in the declining of mental functions. Posterior Cortical Atrophy is referred to as the loss of brain cells within the outer layer of the brain, mainly affecting the area in the back of the head, where visual information is processed.

Paraneoplastic neurologic syndromes (PNS) are syndromes that result from dysfunction of the nervous system, caused by a benign or malignant tumor via mechanisms other than direct tumor cell infiltration, metastasis, coagulopathy, infection or any treatment side effects [1]. All parts of the central and peripheral nervous system may be affected by PNS and, as a result, signs and symptoms are diverse. Most PNS of the central nervous system have in common a subacute course leaving the patients severely disabled in weeks to months and inflammatory changes in the CSF, including moderate lymphocytic pleocytosis, increased protein levels and IgG index and presence of CSF-specific oligoclonal bands[2]. Early recognition may be difficult

There was a girl named ashley when she was 6 years old she was diagnosed with static encephalopathy, a condition in which her brain is in a forever changing state. Ashleys parents had two other children who were healthy. They had cared for ashley at home since her birth. She could not sit up, use language, roll over, or keep her head up. When she got older it was hard for them to handle her needs. They wanted ashley to have a hysterectomy and they wanted to have hormone therapy.

  FA's major neurological symptoms include muscle weakness and loss of  balance and coordination. FA mostly affects the spinal cord and the

PML is a rare brain demyelinating pathology, characterized by the infection of glial cells, affecting predominantly adults and only occasionally children. Patients have neuropsychological deficits at the time of the onset of the disease. Common symptoms are: motor deficits, altered state of consciousness, visual disturbances and ataxia. However, there are also atypical manifestations that include cerebellar syndrome, meningitis, and meningoencephalitis, progressive myoclonic ataxia, muscular degeneration associated with signs extrapyramidal (Fig.).

Primary progressive MS (PP-MS): Fitzner, D., et al (2010) stated that PP-MS affects nearly 15% of the MS patients. Characterized by the steady progressive deterioration of the neurological function without preceding remissions or relapses. Patients may experience temporary plateaus during which symptoms declines. However, the overall progression of the disability

CMT occurs when there are mutation in genes which encode proteins. Depending on the location and type of gene it effects a different cell, structure or organelle will be effected. It can effect myelin, axons and Schwann cells, the effect can range from compaction and maintenace of myelin, cytoskeletal formation, axonal transport and mitochondrial