Pathophysiology week 7

Where’s My Hand

Like a computer, the brain, the main central processing unit (CPU), vital to all the body organs, is responsible for all the body’s involuntary functions such as heart beat, breathing to a hard-drive for our memories. The video card is our eyes. The sound card is our ears and voice. The skeletal system is the motherboard. The muscular system is the Mega Hertz. The circuits are the nervous system. The power supply unit is the heart. The internet is the environment. All of the above mentioned are connected to brain (CPU) by the nervous system (circuits) supported by the skeletal system (the motherboard) and communicated by neurons (binary code). As one can see, the brain is complex. It receives, processes, and responds, voluntary (somatic nervous system) and involuntary(autonomic nervous system), to all input in order to maintain the body’s homeostasis status.
Cerebrovascular accident (CVA) is a disruption in the oxygenated blood flow to part of the brain due to clogged or rupture artery, causing tissue necrosis. When arteries are unable to carry oxygen and nutrition to the brain tissue due to constriction, obstruction, or rupture, the cells/nerves die (infarct) in areas affected. Infarctions in CVAs are caused by either two means, ischemic or hemorrhage. One type of eschemic CVA is thrombolic, cause by a gradual narrowing or constriction due to atherosclerosis in the cerebral artery. Thrombolic CVAs often occur at rest and at times may be preceded with small transient ischemic attacks. The area of brain affected is usually localized, causing less permanent damage if circulation is restored. Another cause of CVA eschemia is due to an embolus (total obstruction). The event with a embolus is sudden and may occurred from a thrombi created by a myocardial infarction, atherosclerosis, air, tumor or infection. The most destructive (more distributed) type of CVA is the hemorrhagic. The destruction is sudden, can occur with activity, and is more severe. Major cause of hemorrhage CVA is severe hypertension which eventually causes weakening of the blood vessels (arteries and veins) to rupture and causing the intracerebral hemorrhage. Increase intracranial pressure is seen with hemorrhage due to the accumulation of blood, along with edema.. The following case is an example of a how hypertension became a risk factor for CVA. (medscape), (Gould, B. E., pg .485-486., 2011) (Gould, B. E., pg 486-488, 2011)
Robert is a 67 y.o. male who has a history of hypertension. He is a retired executive ans can be found in his garden on most days. One day as he was working in his garden, he begins to notice numbness in his right hand. He tries to finish, but the numbness is spreading. He goes into the house and tries to talk to his wife, but is unable to get the words out. She calls 911 and he is rushed to the hospital. He is admitted to the hospital with a Cerebrovascular Accident. (, 2012)
Over the next two days, Robert symptoms increase. He is given glucocorticoids, but not tissue plasminogen activator (tPA). He is put on oxygen. After 3-4 days, Robert is once again able to speak a few words, but his left upper and lower extremities are flaccid. (, 2012)
The insult of the CVA hemorrhage in Robert’s case more then likely caused cerebral edema, which increases in the infarction area during the first 48 to 72 hours. At the same time, inflammation can also cause increase functional neurological deficits in the first 48 hours before it subsides. After this period, some unaffected neurons around the neurotic tissue will start to recover. Robert’s inflammation and brain swelling (edema) was reduced by the administration of intravenous glucocorticoids. Robert did not receive a medication such as tissue plasminogen activator (tPA), because this is a clot-busting agent and would cause increase bleeding in hemorrhagic cases. (, 2012) (Gould, B. E., pg .485-486., 2011) (Gould, B. E., pg 486-488, 2011)
The real question that needs answering is which side of the brain that the CVA impaired. Considering the initial CVA hemorrhagic insult, Robert’s first experienced right hand numbness that quickly started to spread until he was unable to get words out when talking to his wife. At this point, evidence would point to the brain’s left-side hemisphere. Three to four days later, Robert was able to speak just a few words, however it was not noted exactly how much aphasic impact Robert had. Flaccidity (absent of tone) in Robert’s left upper and lower extremities point to the possible insult to the lower motor neurons in the corticospinal tract or the nuclei of the cranial nerves. During the first couple days after the initial CVA insult, it is also possible the hemorrhage insult has effected adjacent motor area in the brain right hemisphere causing the left upper and lower flaccidity.
Most times flaccidity in affected extremities do not stay in a flaccid state, regardless of mobility issues . Over several weeks after the initial a CVA insult, spastic paralysis can develop. This is why rehabilitation in Robert’s case is so important to initiated as soon as possible. Inactivity can enhance loss of muscle strength, endurance, flexibility and function resulting in abnormal fixation or contractures. (, 2012) (Gould, B. E., pg .485-486., 2011) (Gould, B. E., pg 486-488, 2011)
Rehabilitation treatment for Robert’s recovery has to be a team effort in order to develop a comprehensive program that can be initiated as soon as Robert becomes stable. The team’s goal will be directed in regaining individual function potential, minimizing complications, and accommodating any losses based on Robert’s deficits and strengths. It appears Robert’s hemorrhagic CVA impacted part of his brain’s left-side hemisphere and part of his right-side hemisphere. The deficits that occurred in his brain’s right-side hemisphere caused his left lower and upper extremities to become flaccid (loss of muscle tone) or left-side hemiplegia. Robert’s brain’s left-side hemisphere controls his language and speech abilities. (, 2012) (Gould, B. E., pg .485-486., 2011) (Gould, B. E., pg 486-488, 2011)
Physical therapist will work on his motor functions such as strength, endurance,coordination, and balance. He/she will focus initially on prevention on contractures with bed side passive range of motion,along with a combination of stretching and splinting. The physical therapist may also use supportive braces for arms and hands (helps with alignment and prevents contractures) and a foot-board or tennis shoe worn in bed to prevent foot drop. Eventually, the therapist may reproach Robert’s balance stature when he is in a sitting position. Sitting-balance exercises exposes Robert in strengthening his trunk musculature. Robert’s physical therapist may also promote Robert’s awareness to his deficit side during his routine exercise using compensatory techniques. (, 2012)
The occupation therapist will focus on fine motor functions and upper extremities with emphasis Robert’s self-cares and daily routines that includes hygiene, getting dress, and using the toilet. The occupational therapist main goal is to help Robert gain as much independence in his self cares.
The speech therapist will focus on Robert’s language deficits, teaching him how to strengthen his speech patterns and communicate in other ways. The therapist may also work on any cognitive deficits such a decision making or social skills. Finally Robert’s language therapist will help with swallowing difficulties by encouraging mouth and tongue exercise. Weakness and loss of coordination of swallowing may impair the swallowing (dysphasia) which could cause Robert to aspirate liquid or food. Social worker becomes the Robert’ s advocate-resource person by helping coordinate services and when the time arrives, help ease transitions from hospital to home or into a extended care facility. He/she may be very helpful by counseling Robert and his wife during the challenging rehabilitation period. (, 2012) (Gould, B. E., pg .485-486., 2011) (Gould, B. E., pg 486-488, 2011)

Anonymous. (2012). Stroke Symptoms
Retrieved February 12, 2012, from website

Anonymous. (2012). Motor Recovery in Stroke
Retrieved February 12, 2012, from website

Gould, B. E. (2011) Chapter 22
(pp. 485-488), Path physiology for the Health Professions, 4th Edition. Saunders Learning, printed in United States.

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