[vc_row row_type=”row” use_row_as_full_screen_section=”no” type=”full_width” oblique_section=”no” text_align=”left” css_animation=””][vc_column][ultimate_heading main_heading=”Candidate brief” main_heading_color=”#000000″ sub_heading_color=”#000000″ main_heading_style=”font-weight:bold;” main_heading_font_size=”desktop:36px;”]”This elderly patient has longstanding limb weakness. What is the spot diagnosis?”[/ultimate_heading][vc_empty_space image_repeat=”no-repeat”][vc_video link=”https://vimeo.com/149509069″][vc_empty_space image_repeat=”no-repeat”][vc_row_inner row_type=”row” type=”full_width” use_row_as_full_screen_section_slide=”no” text_align=”left” css_animation=””][vc_column_inner width=”1/4″][stat_counter icon_size=”32″ counter_title=”Station time” counter_value=”20″ counter_suffix=” minutes” speed=”3″][/vc_column_inner][vc_column_inner width=”1/4″][stat_counter icon_size=”32″ counter_title=”Time for this encounter” counter_value=”10″ counter_suffix=” minutes” speed=”3″][/vc_column_inner][vc_column_inner width=”1/4″][stat_counter icon_size=”32″ counter_title=”Maximum time to examine your patient” counter_value=”8″ counter_suffix=” minutes” speed=”3″][/vc_column_inner][vc_column_inner width=”1/4″][stat_counter icon_size=”32″ counter_title=”Minimum time for discussion and questions” counter_value=”2″ counter_suffix=” minutes” speed=”3″][/vc_column_inner][/vc_row_inner][vc_empty_space image_repeat=”no-repeat”][/vc_column][/vc_row]
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This patient has longstanding muscle wasting of their left leg. As they are elderly, the likely diagnosis is post-polio syndrome.
Poliovirus – Long-Term Sequelae
Poliovirus enters and multiples in the oropharynx, with an incubation period of 2-35 days. Transmission is via the fecal-oral route. The poliovirus’ high affinity for the CD155 receptor allows the virus to spread to the CNS by afferent nerve pathways.
Neurodegeneration of the anterior horn cells of spinal cord results in limb paralysis. The virus may also spread to posterior horn cells, thalamus, hypothalamus and even in the brain stem, which can be fatal. In severe cases, the cause of death is attributed to respiratory paralysis.
The neurohistopathology of affected motor neurons reveals vacuolation, axonal deterioration, and the accumulation of polymorphonuclear neutrophils and microglia.
Over 2/3 of patients with paralytic polio develop symptoms of postpolio syndrome (PPS). PPS is a new, insidious onset of weakness, fatigue and pain with additional muscle atrophy years after the acute infection. The progressive muscle atrophy of PPS is probably due to ongoing motor neuron degeneration.
The diagnosis of PPS is based on neurophysiological findings in conjunction with the exclusion of other diseases that could produce the same constellation of symptoms.
Risk factors for the development of PPS include original polio severity, disease onset in adolescence or adulthood, and paradoxically, a good recovery. The syndrome is also more common in women and increases with time after acute poliomyelitis.
Electromyography in this patient population can be used to confirm the history of acute poliomyelitis. However, there are no definitive tests for PPS. The symptomatology of PPS is qualitative but characteristic and clinically recognizable:
Excessive fatigue that worsens as the day goes on, with flu-like aching, exercise intolerance, and diminished endurance.
Joint and muscle pain affects more than 2/3 of patients with PPS. Patients will complain of a deep aching pain that is exacerbated by extreme temperatures.
Muscle weakness can occur in muscles originally affected by polio or in muscles that did not appear weak during the first episode.
Patients also complain of cold interlace (29-56%), difficulty swallowing (10-20%), and psychological stress (62-70%).
Joint deterioration and skeletal deformities can substantially impinge on quality of life and result in long-term occupational disability.
The development of PPS is attributed to the progressive degeneration of motor neurons that previously compensated for neurons destroyed during the original infection. An ongoing cycle of denervation and reinnervation, where compensatory reinnervation begins to fail, is also implicated.
The reactivation of the original poliovirus infection is not thought to play a role. However, a minority of researchers have proposed that a neuroinflammatory milieu arises from a persisting polioviruses infection in the brain that primes patients for the development of PPS.
Rehabilitation of patients with PPS is multidisciplinary, involving physiotherapy, muscle training and tailored physical activity regimens to avoid both inactivity and overuse of weak muscles.
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