This man is suffering from acute inflammatory demyelinating polyradiculoneuropathy (AIDP), also known as Guillain-Barre Syndrome. As suggested by the name, the pathology is due to demyelination.

AIDP is a symmetric ascending paralysis that begins in the feet and ascends to the trunk and upper extremities. The paralysis will often impair breathing and frequently affects the facial nerve as well. This disease commonly follows an illness, especially infectious diarrhea caused by Campylobacter jejuni. The immune response to foreign antigens mistakenly targets host nerve tissues, specifically the myelin sheaths.

Inhibition of ACh release into synaptic cleft can also result in weakness, but describes the effects of botulinum toxin in botulism. The toxin is made by the bacteria Clostridium botulinum as a foodborne illness. Patients experience weakness, trouble seeing, fatigue, and possible speech difficulties. Muscular weakness may follow. Diagnosis is made by identifying the toxin in food or feces.

Blockade of action potentials is seen in conduction blockages as a result of nerve injury, such as neuropraxia, axonotmesis, or neurotmesis.

Blockade of presynaptic voltage-gated calcium channels describes Lambert-Eaton Syndrome, a presynaptic neuromuscular junction disorder characterized by muscular weakness of the limbs. It is an autoimmune condition that attacks presynaptic voltage-gated calcium channels. Proximal muscles are affected first, so patients have difficulty climbing stairs or standing up from sitting. They also may have difficulty reaching over their head or combing their hair. Diagnosis is made by EMG, which shows normal latency and conduction velocities, but small amplitudes. Rapid bursts of stimuli or exercising the muscle will lead to greatly increased amplitudes due to an influx of calcium.

Blockade of postsynaptic ACh receptors is seen in myasthenia gravis, a postsynaptic neuromuscular junction disorder very similar to Lambert-Eaton Syndrome. It is an autoimmune disorder directed against postsynaptic acetylcholine receptors and is characterized by easy fatigue. Muscles become progressively weaker with activity, so patients tend to have symptoms at the end of the day. Earliest signs include difficulty keeping the eyes open, or difficulty with chewing, speaking, or swallowing. EMG studies will show progressively decreasing amplitudes with repeated stimuli.

You would expect decreasing amplitude with repeated stimulation.

This woman is suffering from myasthenia gravis, a postsynaptic neuromuscular junction disorder. It is an autoimmune disorder directed against postsynaptic acetylcholine receptors and is characterized by easy fatigue. Muscles become progressively weaker with activity, so patients tend to have symptoms at the end of the day. Earliest signs include difficulty keeping the eyes open, or difficulty with chewing, speaking, or swallowing.

Increasing amplitude would be seen in Lambert-Eaton Syndrome, a presynaptic neuromuscular junction disorder characterized by muscular weakness in the limbs. It is an autoimmune condition that attacks presynaptic voltage-gated calcium channels. Proximal muscles are affected first and patients have difficulty climbing stairs or standing up from sitting. They also may have difficulty reaching over their head or combing their hair. Rapid burst of stimuli or exercising the muscle will lead to greatly increased amplitudes due to an influx of calcium.

Fibrillations are seen with axonal injury.

Left untreated, you can expect the patient to develop hypotonia.

First, let's diagnose the patient. She complains of symmetric lack of feeling in her upper extremities, specifically inability to distinguish temperature. This is a classic description of syringomyelia, a pathology in which a cyst or cavity forms within the center of the cervical spinal cord. This disrupts the anterior white commissure and crossing spinothalamic tracts, leading to loss of pain and temperature sensation in the upper back, upper chest, and upper extremities.

Cavitation will appear as a "density" or darkness on T1 MRI. Left untreated, cavitation or cysts may extend to involve the anterior horn, which will result in a lower motor neuron disease. Lower motor neuron disease is characterized by hypotonia (low muscle tone), muscle atrophy, flaccid paralysis, areflexia, fasciculations, and fibrillations on EMG.

Clonus is involuntary, rhythmic movements of a muscle group that is seen in upper motor neuron (UMN) disease. Clasp-knife spasticity is also seen in UMN disease and is described as initial resistance to passive flexion of a joint, followed by a sudden decrease in resistance. Also seen in UMN disease is hyperreflexia, spastic paralysis, and Babinski sign—fanning out of the toes after stroking the bottom of the foot. Loss of vibration and proprioception is seen with involvement of the dorsal column of the spinal cord.

Wernicke's area is a portion of the temporal lobe that helps formulate and understand speech. Damage to this area results in patients that are able to talk easily, but have little to no meaning in their speech. Damage to Broca's area would result in the inability to produce speech. Olfactory damage would result in the inability to smell and damage to the motor cortex would result in spontaneous and inappropriate movements. 

Drop foot is observed as an unusual gait, where the foot drops due to weakness in the tibialis anterior, and associated dorsiflexors, or to damage to the deep fibular nerve. The deep fibular nerve innervates the anterior compartment of the lower leg, where the dorsiflexors originate. Injury to this nerve would make a person unable to dorsiflex her ankle, causing it to drag/present as a drop foot.

Tarsal tunnel syndrome occurs when the tibial nerve is compressed against the flexor retinaculum of the foot and or portions of the talus and calcaneus, as these three structures comprise the tarsal tunnel. Typically, patients with tarsal tunnel syndrome will report numbness, pain, and/or a tingling sensation radiating to the hallux.

The axillary nerve is most commonly injured in shoulder dislocations. The radial nerve is more commonly injured in humerus fractures, the long thoracic nerve is more commonly injured with traction injuries, the accessory nerve is more commonly injured iatrogenically (during surgery), and the sciatic nerve is more commonly injured as a result of vertebral misalignment.

A Brown-Séquard lesion affects half of the spinal cord. Because the spinothalamic tracts decussate at or near the vertebral level they provide sensation too, injury to them would cause contralateral deficits in pain and temperature sensation. By the same principle, the dorsal column medial lemniscus does not decussate until it reaches the medulla, so injury to this tract would cause ipsilateral loss of proprioception and vibration sense. Eye movements and hearing are controlled by cranial nerves, so a spinal cord lesion would not affect them. This leaves ipsilateral motor loss as the correct choice.

The long thoracic nerve (C5-C7) innervates the serratus anterior, which connects the scapula to the thorcaic cage. It is also used for abduction above the horizontal position. During a mastectomy this nerve can be injured leading to a "winged" scapula. A winged scapula is a condition in which the shoulder blade protrudes from a person's back in an abnormal position leading to limited functional activity in the adjacent upper extremity.

SMA involves atrophy of skeletal muscles. Werdnig-Hoffmann disease is synonymous with SMA type I, which involves severe, early onset (first few months of birth) SMA. Dubowitz disease is synonymous with SMA type II (intermediate), which involves onset at around 6-18 months age. Kugelberg-Welander disease, also known as juvenile SMA, is synonymous with SMA type III, and involves the affected individual being able to walk without support at some time, but the probable loss of this ability later in life. SMA type IV does not have an associated eponym, and there is no SMA type V.