Physician Assistant National Certifying Examination (PANCE) Neurology and Behavioral Health Syllabus

What is the pathologic hallmark and earliest clinical feature of Alzheimer disease?

Pathology: extracellular beta-amyloid plaques and intracellular neurofibrillary tangles (hyperphosphorylated tau). Earliest clinical feature: short-term/episodic memory loss (anterograde amnesia).

Contrast vascular dementia, Lewy body dementia, and frontotemporal dementia by their distinguishing features.

Vascular: stepwise decline with focal deficits/stroke history. Lewy body: fluctuating cognition, visual hallucinations, parkinsonism, REM sleep behavior disorder, antipsychotic sensitivity. Frontotemporal: early personality/behavioral change and language deficits with relatively preserved memory.

Which two medication classes are used to slow symptomatic progression of Alzheimer dementia?

Cholinesterase inhibitors (donepezil, rivastigmine, galantamine) for mild-moderate disease, and the NMDA-receptor antagonist memantine for moderate-severe disease.

What is the hallmark imaging and clinical pattern of multiple sclerosis (MS)?

MS is a demyelinating CNS disease with lesions 'separated in space and time.' MRI shows multiple periventricular white matter plaques (ovoid, Dawson fingers). CSF shows oligoclonal bands.

What are common presenting symptoms of multiple sclerosis?

Optic neuritis (painful monocular vision loss), internuclear ophthalmoplegia, sensory disturbances, limb weakness, Lhermitte sign (electric shock down spine with neck flexion), and Uhthoff phenomenon (symptom worsening with heat).

What is the treatment of an acute MS relapse versus long-term disease modification?

Acute relapse: high-dose IV corticosteroids (methylprednisolone). Long-term: disease-modifying therapies (e.g., interferon-beta, glatiramer acetate, natalizumab, ocrelizumab, fingolimod).

How does essential tremor differ from the tremor of Parkinson disease?

Essential tremor is a bilateral ACTION/postural tremor (worse with movement, improves with alcohol, often familial). Parkinson tremor is a RESTING tremor that improves with movement. Essential tremor is treated with propranolol or primidone.

What are the inheritance pattern and clinical features of Huntington disease?

Autosomal dominant CAG trinucleotide repeat expansion (HTT gene) with anticipation. Features: chorea, behavioral/psychiatric changes, and progressive dementia, typically beginning in middle age. MRI shows caudate atrophy.

What is the classic clinical pattern of diabetic peripheral neuropathy?

Distal symmetric 'stocking-glove' sensory loss (length-dependent), often with burning/tingling pain, beginning in the feet. It is the most common cause of peripheral polyneuropathy.

What is the classic presentation of Guillain-Barre syndrome (GBS)?

Acute, ascending, symmetric flaccid paralysis with areflexia, often following a respiratory or GI infection (e.g., Campylobacter jejuni). It is an acute inflammatory demyelinating polyneuropathy.

What are the characteristic CSF and treatment findings in Guillain-Barre syndrome?

CSF shows albuminocytologic dissociation (elevated protein with normal WBC count). Treatment: IVIG or plasmapheresis. Monitor respiratory function (vital capacity) closely; corticosteroids are NOT effective.

What is the underlying mechanism and hallmark symptom of myasthenia gravis?

Autoantibodies against postsynaptic acetylcholine receptors at the neuromuscular junction. Hallmark: fatigable muscle weakness that WORSENS with use/throughout the day, often with ptosis and diplopia.

How is myasthenia gravis diagnosed and treated?

Diagnosis: acetylcholine receptor (AChR) antibodies, edrophonium (Tensilon) test, repetitive nerve stimulation showing decremental response, and chest CT for thymoma. Treatment: acetylcholinesterase inhibitors (pyridostigmine), immunosuppression, and thymectomy.

Contrast myasthenia gravis with Lambert-Eaton myasthenic syndrome.

Myasthenia gravis: postsynaptic AChR antibodies; weakness WORSENS with use; ocular symptoms prominent. Lambert-Eaton: presynaptic voltage-gated calcium channel antibodies (often paraneoplastic with small cell lung cancer); weakness IMPROVES with repeated use; autonomic symptoms common.

How do you distinguish a peripheral (Bell palsy) facial nerve lesion from a central (stroke) facial weakness?

Bell palsy (peripheral CN VII) affects the ENTIRE half of the face, including the forehead. Central lesions (e.g., stroke) SPARE the forehead because of bilateral cortical innervation of the upper face.

What is the treatment for Bell palsy and a key supportive measure?

Corticosteroids (prednisone) started early, +/- antivirals if herpes/Ramsay Hunt is suspected. Key supportive care: eye lubrication and patching to prevent corneal abrasion/exposure keratopathy (impaired eye closure).

Which cranial nerve is affected in trigeminal neuralgia, and what is the first-line treatment?

Cranial nerve V (trigeminal). It causes brief, severe, lancinating unilateral facial pain triggered by light touch. First-line treatment: carbamazepine.

What are the DSM-5 criteria duration thresholds for a major depressive episode versus persistent depressive disorder (dysthymia)?

Major depressive episode: $\geq 5$ symptoms (including depressed mood or anhedonia) for $\geq 2$ weeks. Persistent depressive disorder (dysthymia): depressed mood most of the day, more days than not, for $\geq 2$ years (1 year in children/adolescents).

Recall the SIGECAPS mnemonic used to assess for major depressive disorder.

Sleep changes, Interest loss (anhedonia), Guilt/worthlessness, Energy loss, Concentration difficulty, Appetite/weight changes, Psychomotor agitation/retardation, Suicidality. Plus depressed mood — need $\geq 5$ for $\geq 2$ weeks.

How is bipolar I disorder distinguished from bipolar II disorder?

Bipolar I requires at least one full MANIC episode ($\geq 7$ days or hospitalization). Bipolar II requires at least one HYPOMANIC episode ($\geq 4$ days) plus at least one major depressive episode, with NO full manic episode.

What is first-line pharmacotherapy for major depressive disorder, and how long until full effect?

Selective serotonin reuptake inhibitors (SSRIs). Full therapeutic effect typically takes 4-6 weeks, though some improvement may begin earlier.

What defines generalized anxiety disorder (GAD) in the DSM-5?

Excessive anxiety and worry about multiple events/activities, more days than not, for $\geq 6$ months, that is difficult to control, with $\geq 3$ associated symptoms (restlessness, fatigue, difficulty concentrating, irritability, muscle tension, sleep disturbance).

How does a panic attack present, and what defines panic disorder?

A panic attack is an abrupt surge of intense fear peaking within minutes with somatic symptoms (palpitations, chest pain, dyspnea, dizziness, fear of dying). Panic disorder = recurrent unexpected panic attacks plus $\geq 1$ month of worry about future attacks or maladaptive behavior change.

What distinguishes obsessions from compulsions in OCD?

Obsessions are recurrent, intrusive, unwanted thoughts/urges causing anxiety. Compulsions are repetitive behaviors or mental acts performed to reduce that anxiety. First-line treatment: SSRIs (often higher doses) and exposure-response prevention therapy.

How is PTSD distinguished from acute stress disorder?

Both follow exposure to trauma with intrusion, avoidance, negative mood/cognition, and arousal symptoms. Acute stress disorder lasts 3 days to 1 month; PTSD requires symptoms persisting $> 1$ month.

What are the DSM-5 symptom categories required for diagnosing schizophrenia, and the duration?

$\geq 2$ of: delusions, hallucinations, disorganized speech, grossly disorganized/catatonic behavior, negative symptoms (at least one must be one of the first three), with continuous signs for $\geq 6$ months (including $\geq 1$ month of active symptoms).

Differentiate schizophrenia, schizophreniform disorder, and brief psychotic disorder by duration.

Brief psychotic disorder: symptoms 1 day to $< 1$ month with full return to baseline. Schizophreniform: 1 to 6 months. Schizophrenia: $\geq 6$ months total.

Contrast positive and negative symptoms of schizophrenia and their treatment responsiveness.

Positive symptoms (hallucinations, delusions, disorganized speech) respond well to antipsychotics. Negative symptoms (flat affect, alogia, avolition, anhedonia, social withdrawal) respond poorly and are managed better by atypical (second-generation) antipsychotics.

What is the CAGE questionnaire used to screen for, and what does a positive result require?

It screens for alcohol use disorder. Questions: Cut down, Annoyed by criticism, Guilty about drinking, Eye-opener (morning drink). $\geq 2$ positive answers suggests problematic drinking warranting further evaluation.

Describe the timeline and danger of alcohol withdrawal, including delirium tremens.

Tremor/anxiety begin 6-24 hours after last drink; withdrawal seizures 12-48 hours; delirium tremens (DTs) at 48-96 hours with autonomic instability, confusion, and hallucinations. DTs can be fatal. Treatment: benzodiazepines and thiamine (before glucose).

What medications are used for opioid use disorder maintenance, and which opioid overdose reversal agent is used?

Maintenance: methadone (full agonist), buprenorphine (partial agonist, often with naloxone), and naltrexone (antagonist). Acute overdose reversal: naloxone (an opioid receptor antagonist).