Progressive supranuclear palsy is a rare disease that continuously 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 worsens as the illness progresses. The palsy has effects on capability to move the eyes, relax the muscles, and control balance.
Progressive supranuclear palsy is a disease of middle age. Symptoms usually begin in the 60s, infrequently before age 45 or after age 75. Men develop PSP more often than girls do. It has effects on 3 to four folks per million every year.
Prognosis for progressive supranuclear palsy: affects the brainstem, the basal ganglia, and the cerebellum. The brainstem is located at the apex of the spinal nerve. It controls the most elementary functions required for survival-the involuntary ( unwilled ) movements such as breathing, blood pressure, and pulse rate. The brainstem has three parts : the medulla oblongata, the pons, and the midbrain. The parts affected by PSP are the pons, which controls facial nerves and the muscles that turn the eye outward, and the midbrain, the visible center. The fundamental 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 difficulty only happens in trying to look down. As the disease moves on, ability to move the eyes right and left is also affected. However reflex or unwilled eye movements remain normal. Thus, when the patient’s head is tilted upwards, the eyes move to look down. These reflex movements remain standard till late in the course of the illness. The higher eyelids could be pulled back, the eyebrows raised, and the brow wrinkled, causing a normal wide-eyed stare. Rate of blinking may fall from the normal 20-30 per minute to three to 5 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 signs of PSP could be frequent falls or stiff, slow movements of the arms and legs. These symptoms may appear as much as 5 years before the characteristic vision issues. Walking becomes increasingly ungainly, and some patients tend to lean and fall backward. Facial muscles could be puny, causing slurred speech and difficulty swallowing. Sleep may be disturbed and thought processes slowed. Although memory remains intact, the slowed speech and thought patterns and the rigid facial expression might be mistaken for senile dementia or Alzheimer’s disease. Emotional responses may become exaggerated and unbecoming, and the patient may experience anxiety, depression, and agitation.
The cause of PSP is not known. The majority who develop PSP come from families with no history of the disease, so it doesn’t appear to be inherited, except in certain rare examples. 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. Transmitting structures in brain cells called neurofibrils become disorganised ( neurofibrillary tangles ). Neurofibrillary tangles are also found in Alzheimer’s disease, but the pattern is somewhat different. Check out also cerebral palsy information.
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