Progressive supranuclear palsy is a rare disease that gradually destroys nerve cells in the parts of the brain that control eye movements, breathing, and muscle coordination. The loss of nerve cells causes palsy, or paralysis, that slowly gets worse as the illness moves on. The palsy affects capability to move the eyes, relax the muscles, and control balance.
Progressive supranuclear palsy is an illness of middle age. Symptoms generally begin in the 60s, infrequently before age 45 or after age seventy five. Men develop PSP more frequently than girls do. It is affecting 3 to four folk per million annually.
Progressive supranuclear palsy prognosis: is affecting the brainstem, the fundamental ganglia, and the cerebellum. The brainstem is located at the top of the spinal cord. It controls the most simple functions needed for survival-the involuntary ( unwilled ) movements like respiring, blood pressure, and heart rate. The brainstem has three parts : the medulla oblongata, the pons, and the midbrain. The parts impacted by PSP are the pons, which controls facial nerves and the muscles that turn the eye outward, and the midbrain, the visual center. The basal ganglia are islands of nerve cells located deep within the brain. They are involved in the initiation of voluntary ( willed ) movement and control of emotion. Damage to the basal ganglia causes muscle rigidity ( spasticity ) and shocks. The cerebellum is found at the base of the skull. It controls balance and muscle coordination.
Vision is controlled by groups of cells called nuclei in the brainstem. In PSP, the nuclei continue to function, but the mechanisms that control the nuclei are destroyed. The term supranuclear implies the damage is done above ( supra ) the nuclei. Patients with PSP have trouble with voluntary ( willed ) eye movement. Initially, the problem only occurs in attempting to look down. As the disease advances, ability to move the eyes right and left is also influenced. However reflex or unwilled eye movements remain ordinary. Thus, when the patient’s head is angled upwards, the eyes move to look down. These reflex movements remain ordinary until late in the course of the illness. The higher eyelids could be pulled back, the eyebrows raised, and the brow wrinkled, causing a typical wide-eyed stare. Rate of blinking may decline from the normal 20-30 per minute to three to five per minute. It becomes tough to walk downstairs, to maintain eye contact during conversation, or to move the eyes up and down to read.
The earliest evidence of PSP could be frequent falls or stiff, slow movements of the legs and arms. These symptoms may appear as much as 5 years before the characteristic vision issues. Walking becomes very clumsy, and some patients tend to lean and fall backward. Facial muscles might be feeble, causing slurred speech and difficulty swallowing. Sleep may be troubled and thought processes slowed. Although memory remains intact, the slowed speech and thought patterns and the rigid facial appearance could be mistaken for senile dementia or Alzheimer’s illness. Emotive reactions may become exaggerated and inappropriate, and the patient may experience anxiety, depression, and agitation.
The cause of PSP isn’t known. Most of the people who develop PSP come from families with no history of the disease, so it does not seem to be inherited, except in certain rare instances. People who have PSP seem to lack the neurotransmitters dopamine and homovanillic acid in the basal ganglia. Neurotransmitters are chemicals that help carry electric impulses along the nervous system. Broadcasting structures in brain cells called neurofibrils become disorganized ( neurofibrillary tangles ). Neurofibrillary tangles are also found in Alzheimer’s disease, but the pattern is rather different. Check out also cerebral palsy info.
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