Post-Polio Syndrome and Recovery Quiz

<p>20% to 85% (B)</p> Signup and view all the answers

<p>Using ligaments for stability (A)</p> Signup and view all the answers

<p>Amyotrophic Lateral Sclerosis (C)</p> Signup and view all the answers

<p>Progressive muscular atrophy (B)</p> Signup and view all the answers

<p>9.9 per 100,000 adults (C)</p> Signup and view all the answers

<p>1.6 persons per 100,000 (B)</p> Signup and view all the answers

<p>Muscle weakness without atrophy (B)</p> Signup and view all the answers

<p>Mid to late 50s (A)</p> Signup and view all the answers

<p>5% to 10% (A)</p> Signup and view all the answers

<p>C9ORF72 gene (C)</p> Signup and view all the answers

<p>Muscle weakness (B)</p> Signup and view all the answers

<p>Riluzole (C)</p> Signup and view all the answers

<p>To exclude other causes (B)</p> Signup and view all the answers

<p>Cognitive impairment (A)</p> Signup and view all the answers

<p>4.08 years (D)</p> Signup and view all the answers

<p>Rapid onset of symptoms (D)</p> Signup and view all the answers

<p>Higher rates of development (D)</p> Signup and view all the answers

<p>Spasticity (C)</p> Signup and view all the answers

<p>Progression of signs and symptoms (A)</p> Signup and view all the answers

<p>Managing the respiratory function (C)</p> Signup and view all the answers

<p>Fatigue (B)</p> Signup and view all the answers

<p>Infection from new polio virus (C)</p> Signup and view all the answers

<p>15 to 30 years (B)</p> Signup and view all the answers

<p>Asymmetric weakness (D)</p> Signup and view all the answers

<p>At least 15 years (A)</p> Signup and view all the answers

<p>Those with residual respiratory muscle weakness (B)</p> Signup and view all the answers

<p>Deep high-intensity pain (A)</p> Signup and view all the answers

<p>Denervation exceeding reinnervation (B)</p> Signup and view all the answers

<p>Electrolyte imbalance (C)</p> Signup and view all the answers

<p>Subclinical weakness in pharyngeal constrictor muscles (B)</p> Signup and view all the answers

<p>Decreased ability for motor neurons to compensate (C)</p> Signup and view all the answers

<p>Multiple Sclerosis (D)</p> Signup and view all the answers

<p>National Rehabilitation Hospital Postpolio Limb Classification (D)</p> Signup and view all the answers

A process where motor neurons that have been damaged by polio recover and regain normal function.

When recovered motor neurons send out new branches (axon sprouts) to connect with muscle fibers that lost their original connection. This creates larger motor units.

The ability to increase the strength and size of muscle fibers that are still connected to a motor neuron. This happens due to intense exercise after nerve damage.

The period in the 1970s and 1980s when polio survivors began to experience new muscle weakness, even in muscles that were not initially affected by polio.

The long-term consequences of using compensatory methods for function after polio. This includes overuse of certain muscles, ligaments, and joints.

A progressive, degenerative neurological disorder affecting both upper and lower motor neurons. It leads to muscle weakness, atrophy, spasticity, and eventually paralysis.

Upper motor neurons (UMNs) control voluntary movement by sending signals from the brain to the spinal cord. Lower motor neurons (LMNs) transmit signals from the spinal cord to the muscles.

A rare disorder affecting only upper motor neurons, causing spasticity and weakness. It primarily impacts the legs and trunk.

A degenerative disease of the motor neurons in the brainstem, affecting cranial nerves IX-XII. It causes difficulties with speech, swallowing, and facial movements.

A neurological disorder characterized by the loss of lower motor neurons, resulting in muscle weakness, atrophy, and fasciculations. It affects the arms and hands first, then spreads to the legs and trunk.

A post-polio syndrome symptom characterized by sudden, overwhelming tiredness, often worse in the late afternoon and evening. It may not improve even after resting.

Affects previously healthy motor neurons, making them unable to maintain new nerve connections. This leads to a mismatch where nerve loss surpasses nerve regeneration.

The inability to initiate and control voluntary movements due to a dysfunction in the brain's motor cortex.

The theory that neurons affected by polio, even if initially recovered, are vulnerable to premature aging and failure due to their prior trauma.

The depletion of the motor neuron pool in polio patients. The motor neurons lost due to aging exacerbate the pre-existing depletion.

The hypothesis that the surviving motor neurons overwork by maintaining excessive connections, leading to their exhaustion.

A difficulty in transmitting signals between nerves and muscles, resulting in muscle fatigue and decreased endurance.

A potential contributor to the development of new muscle weakness in Postpolio Syndrome.

A common symptom of Postpolio Syndrome, often described as intense, deep pain, which may be a contributing factor to myofascial pain or fibromyalgia.

An involuntary muscle contraction that can occur in Postpolio Syndrome, mostly affecting the legs, neck, and shoulders.

The new onset of muscle weakness in previously unaffected muscles, a hallmark of Postpolio Syndrome.

The breakdown of muscle tissue, leading to a decrease in muscle size, a common sign of Postpolio Syndrome.

The progressive loss of muscle strength due to the decline in motor neuron function, a characteristic of Postpolio Syndrome.

Difficulty swallowing, often observed in patients with both bulbar and nonbulbar Postpolio Syndrome.

The deterioration of muscle strength, pain, and joint instability contributing to difficulty maintaining balance and walking.

About 90-95% of ALS cases are sporadic, meaning the cause is unknown. The remaining 5-10% are familial, linked to genetic mutations.

A mutation in the C9ORF72 gene is the most common genetic cause of ALS, accounting for roughly one-third of familial cases. It is also linked to frontotemporal dementia.

A common theory for ALS is that excess glutamate in the central nervous system (CNS) overexcites motor neurons, leading to damage. This is known as glutamate excitotoxicity.

Another theory for ALS is that an accumulation of free radicals in the body can oxidize and damage cell membranes, proteins, and genetic material, leading to cell death.

Abnormal protein clumps found in motor neurons of ALS patients, interfering with normal cell function, is a key feature of the disease.

Impairment of nerve signals from the central nervous system to the muscles due to damage to the upper motor neurons (UMNs). This can lead to spasticity, hyperreflexia, and muscle weakness.

Loss of nerve signals from the spinal cord to the muscles due to lower motor neuron (LMN) degeneration. This causes muscle weakness, atrophy, fasciculations, and hyporeflexia.

Difficulty swallowing, often an early sign of ALS affecting the nerves controlling swallowing.

Difficulty speaking caused by damage to the nerves responsible for speech.

An uncontrolled, involuntary tendency to cry or laugh, often a sign of ALS affecting the brain's emotional centers.

Difficulty breathing, often an advanced symptom caused by ALS's impact on the nerves controlling breathing.

A decline in cognitive abilities including verbal fluency, visual attention, language comprehension, memory, and executive function. It may occur in individuals with ALS.

A variant of frontotemporal dementia affecting personality and behaviour, often observed in ALS patients.

Riluzole (Rilutek, Tiglutik, Exservan) is a medication approved to treat ALS by slowing its progression and protecting motor neurons from damage. It works by reducing glutamate levels.

Edaravone (Radicava) is a neuroprotective drug approved to treat ALS. It slows the decline in physical function by counteracting oxidative stress.