Guillain-Barré syndrome is an inflammatory demyelinating polyneuropathy that affects not only motor nerves but also autonomic nerves. Autonomic dysfunction is a common and potentially life-threatening complication. Manifestations can include cardiac arrhythmias (tachycardia, bradycardia), blood pressure instability (hypertension or hypotension), urinary retention, and ileus. Therefore, patients require continuous cardiac and blood pressure monitoring. Increased intracranial pressure, seizures, and cognitive decline are not typical complications of GBS.

This patient's presentation of fluctuating ptosis, diplopia, and bulbar weakness that worsens with activity is classic for myasthenia gravis (MG). The most appropriate initial test is serologic testing for acetylcholine receptor (AChR) antibodies, which is positive in about 85% of patients with generalized MG and has high specificity. If AChR antibodies are negative, testing for MuSK antibodies should be performed. Repetitive nerve stimulation studies show a decremental response in MG but are less specific and typically used when antibody testing is negative or to confirm the diagnosis functionally. Single-fiber EMG is the most sensitive test but is technically demanding and reserved for cases where other tests are inconclusive. CT scan of the chest to screen for thymoma is important but performed after confirming the diagnosis.

This patient's clinical picture of proximal muscle weakness that improves with activity (Lambert-Eaton facilitation), hyporeflexia, and a history of smoking with a lung mass is highly suggestive of Lambert-Eaton myasthenic syndrome (LEMS), a paraneoplastic syndrome most commonly associated with small cell lung cancer. The pathophysiology of LEMS involves autoantibodies directed against presynaptic P/Q-type voltage-gated calcium channels, which impairs acetylcholine release. Antibodies against postsynaptic ACh receptors cause myasthenia gravis. Antibodies against myelin basic protein are associated with multiple sclerosis, and antibodies against aquaporin-4 are seen in neuromyelitis optica.

This patient presents with the classic triad of Parkinson disease: bradykinesia (slowness, soft voice, small handwriting), resting tremor, and rigidity. Given his age (>65) and significant functional impairment (falls), carbidopa-levodopa is the most effective and appropriate initial treatment. Dopamine agonists like pramipexole are often used in younger patients to delay levodopa-related motor complications but are less effective and have a higher risk of side effects (e.g., hallucinations) in older adults. Benztropine is an anticholinergic used primarily for tremor in younger patients and is poorly tolerated in the elderly. Amantadine offers mild symptomatic benefit but is less potent than levodopa.

This patient has essential tremor, characterized by bilateral action (postural and kinetic) tremor that improves with alcohol and has a positive family history. The two first-line pharmacologic treatments for essential tremor are propranolol (a non-selective beta-blocker) and primidone (an anticonvulsant). Among the choices given, propranolol is the most appropriate. Levodopa is used for Parkinson disease, which typically presents with resting tremor, bradykinesia, and rigidity. Gabapentin may have some efficacy but is considered a second-line agent. Clonazepam can be helpful but is also not first-line due to concerns about sedation and dependence.

The clinical presentation of chorea, psychiatric changes (irritability, impulsivity), and a positive family history is highly suggestive of Huntington disease. This is an autosomal dominant neurodegenerative disorder caused by an expanded number of CAG (cytosine-adenine-guanine) trinucleotide repeats in the huntingtin gene. A point mutation in the copper-transporting ATPase gene (ATP7B) causes Wilson disease. A deletion in the SMN1 gene causes spinal muscular atrophy. A GGGGCC repeat expansion in the C9orf72 gene is the most common genetic cause of amyotrophic lateral sclerosis and frontotemporal dementia.

This patient's presentation with a combination of both upper motor neuron (UMN) signs (hyperreflexia, Babinski signs) and lower motor neuron (LMN) signs (asymmetric weakness, atrophy, fasciculations) is the hallmark of amyotrophic lateral sclerosis (ALS). ALS is a progressive neurodegenerative disease affecting motor neurons. Multiple sclerosis typically presents with sensory deficits and optic neuritis. Myasthenia gravis causes fluctuating weakness without UMN signs. Spinal muscular atrophy is a pure LMN disease and does not cause hyperreflexia or Babinski signs.

This patient's presentation of acute, ascending, symmetric paralysis with areflexia following a recent gastrointestinal infection is characteristic of Guillain-Barré syndrome (GBS). While her vital capacity of 25 mL/kg is concerning and requires close respiratory monitoring, she does not yet require intubation (typically indicated when vital capacity drops below 15-20 mL/kg or with other signs of respiratory compromise). The most appropriate next step is to initiate disease-modifying treatment with intravenous immunoglobulins (IVIG) or plasmapheresis, both of which are equally effective first-line treatments that can halt disease progression. Diagnostic tests like MRI and lumbar puncture can be useful but should not delay treatment in a clinically obvious case.

This patient has restless legs syndrome (RLS). An important secondary cause of RLS is iron deficiency. Before initiating symptomatic treatment with dopamine agonists (e.g., pramipexole) or alpha-2-delta ligands (e.g., gabapentin), it is essential to check iron stores and replete them if low. In patients with RLS and a serum ferritin level <75 ng/mL, oral iron supplementation is recommended as the initial management, as it can significantly improve or resolve symptoms.

This patient has cervical dystonia (spasmodic torticollis), a form of focal dystonia characterized by sustained muscle contractions causing abnormal neck posturing. The ability to temporarily correct the posture with a sensory trick ('geste antagoniste') is a classic feature. The most effective and first-line treatment for focal dystonias is intramuscular injection of botulinum toxin into the affected muscles (e.g., sternocleidomastoid, trapezius). This selectively weakens the overactive muscles, relieving the abnormal posture and pain. Oral medications like baclofen are less effective and have more systemic side effects. IVIG is not indicated. Physical therapy can be a helpful adjunct but is not the primary treatment.