What is bulbar spinal polio?
Bulbar Paralytic Poliomyelitis Bulbar poliomyelitis results from paralysis of muscle groups innervated by the cranial nerves, especially those of the soft palate and pharynx, which may present as dysphagia, nasal speech, and sometimes dyspnea.
What does the bulbar form of polio affect?
In bulbar polio the virus attacks the brainstem, and the nerve centres that control swallowing and talking are damaged. Secretions collect in the throat and may lead to suffocation by blocking the airway. Some 5 to 10 percent of persons afflicted with paralytic polio die, usually…
Why is bulbar polio The worst?
If the polio virus gets into the brain (bulbar), the muscle groups in the chest needed for breathing and swallowing became paralyzed. This was the most feared complication of the disease, and death often occurred at this point.
Which part of spinal cord is affected in poliomyelitis?
Poliomyelitis is a disease of the lower motor neurons that affects the gray matter of the spinal cord, specifically the yen- tral horns.
Which signs are indicative of post polio syndrome?
Symptoms
- Progressive muscle and joint weakness and pain.
- General fatigue and exhaustion with minimal activity.
- Muscle atrophy.
- Breathing or swallowing problems.
- Sleep-related breathing disorders, such as sleep apnea.
- Decreased tolerance of cold temperatures.
What are the signs of post polio syndrome?
Symptoms of post-polio syndrome persistent fatigue (extreme tiredness) muscle weakness. shrinking muscles. muscle and joint pain.
What type of paralysis is observed in poliomyelitis?
The hallmark of paralytic polio is asymmetric paresis or paralysis. The maximal loss of functions is typically seen within 3 to 5 days of onset but may progress for up to 1 week. Legs are more often involved than arms, and proximal muscles of the extremities are more often involved than distal muscles (Figure 7-2).
Is Post-polio an autoimmune disease?
An inflammatory or autoimmune basis to post-polio syndrome has also been proposed. This hypothesis originates from post mortem observations of inflammatory changes in the spinal cord of PPS patients (35, 36). The role of inflammation is also supported by in vivo evidence.
