11.2 Cerebrovascular Disease, TIA, Peripheral Neuropathies & Movement Disorders (Parkinson's)
Key Takeaways
- Acute ischemic stroke requires rapid triage using the BE-FAST algorithm and emergent non-contrast head CT to rule out hemorrhage; intravenous thrombolysis (alteplase or tenecteplase) must be administered within ≤4.5 hours of last known normal (with BP maintained <185/110 mmHg), while endovascular thrombectomy is indicated up to 24 hours for large vessel occlusions (LVO).
- Transient Ischemic Attack (TIA) represents transient neurological dysfunction without acute infarction on neuroimaging; high-risk patients (ABCD2 score ≥4) require immediate hospitalization, urgent vascular imaging (carotid ultrasound/CTA/MRA), cardiac rhythm monitoring, and initiation of Dual Antiplatelet Therapy (DAPT: aspirin + clopidogrel for 21 days) plus high-intensity statin therapy.
- Stroke syndromes match specific vascular territories: Middle Cerebral Artery (MCA) produces contralateral hemiparesis/hemisensory loss (face/arm > leg) and aphasia (dominant) or hemineglect (non-dominant); Anterior Cerebral Artery (ACA) causes leg/foot > arm weakness and abulia; Posterior Cerebral Artery (PCA) produces homonymous hemianopia with macular sparing; Vertebrobasilar strokes cause the '4 D's' (Dizziness, Diplopia, Dysarthria, Dysphagia) and crossed motor/sensory deficits.
- Peripheral neuropathies require systematic clinical distinction: Distal symmetric diabetic polyneuropathy is a length-dependent sensory-predominant axonal loss (screened annually with 10-g monofilament, treated with duloxetine, pregabalin, or gabapentin); Bell's palsy is an acute lower motor neuron CN VII palsy (paralyzing the entire ipsilateral face including the forehead, treated with oral prednisone within 72 hours), contrasting with upper motor neuron stroke which characteristically spares the forehead.
- Parkinson's Disease is a neurodegenerative synucleinopathy featuring the cardinal TRAP tetrad (Tremor [4–6 Hz resting, asymmetric 'pill-rolling'], Rigidity ['cogwheel'], Akinesia/Bradykinesia [masked facies, micrographic handwriting, shuffling gait], and Postural instability); first-line pharmacotherapy is Carbidopa-Levodopa (gold standard; carbidopa blocks peripheral dopamine decarboxylase, minimizing nausea and orthostasis) or dopamine agonists (pramipexole, ropinirole; caution for impulse control disorders).
Last updated: August 2026
Cerebrovascular Disease, TIA, Peripheral Neuropathies & Movement Disorders (Parkinson's)
Neurological conditions in adult and geriatric populations account for immense morbidity, disability, and mortality in primary care. The Adult-Gerontology Primary Care Nurse Practitioner must possess expert competency in identifying acute cerebrovascular emergencies, calculating post-TIA stroke risk, managing long-term secondary prevention, diagnosing compressive and metabolic peripheral neuropathies, and optimizing complex pharmacotherapy for neurodegenerative movement disorders such as Parkinson's disease.
1. Cerebrovascular Pathophysiology: Ischemic Stroke, TIA & Hemorrhage
Cerebrovascular accidents (CVAs) are classified into two major categories:
- Ischemic Stroke (85–87% of cases): Cerebral infarction resulting from focal arterial hypoperfusion, occlusion, or thrombosis.
- Hemorrhagic Stroke (13–15% of cases): Extravasation of blood into brain parenchyma (Intracerebral Hemorrhage [ICH], primarily caused by chronic hypertension or cerebral amyloid angiopathy) or into the subarachnoid space (Subarachnoid Hemorrhage [SAH], primarily caused by ruptured saccular / berry aneurysms).
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| MECHANISTIC CLASSIFICATION OF ISCHEMIC STROKE |
| |
| 1. LARGE ARTERY ATHEROSCLEROSIS (Thrombotic or Artery-to-Artery Embolic) |
| - In situ plaque rupture and thrombosis of internal carotid artery, |
| vertebral artery, or basilar artery. |
| |
| 2. CARDIOEMBOLISM (~25-30% of all ischemic strokes) |
| - Thrombus generated in heart dislodges to intracranial circulation. |
| - Major Causes: Atrial Fibrillation / Flutter (dominant cause), left |
| ventricular mural thrombus post-MI, mechanical prosthetic valves, |
| dilated cardiomyopathy, patent foramen ovale (PFO / paradoxical). |
| |
| 3. SMALL VESSEL OCCLUSION (Lacunar Stroke, ~20%) |
| - Lipohyalinosis and microatheroma of small penetrating deep arteries |
| (lenticulostriate branches of MCA supplying internal capsule/thalamus)|
| - Driven by chronic hypertension and diabetes mellitus. |
| |
| 4. OTHER DETERMINED ETIOLOGIES |
| - Carotid / vertebral artery dissection (young patients, neck trauma), |
| hypercoagulable states (antiphospholipid syndrome), vasculitis. |
| |
| 5. CRYPTOGENIC (Embolic Stroke of Undetermined Source - ESUS) |
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2. Acute Stroke Triage, Emergency Protocols & Reperfusion
The BE-FAST Pre-Hospital & Clinical Screening Tool
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| THE BE-FAST STROKE ALGORITHM |
| |
| B - BALANCE: Sudden loss of balance, ataxia, vertigo, or unsteadiness |
| E - EYES: Sudden visual loss, diplopia, or visual field deficits |
| F - FACE: Facial droop, asymmetric smile, flattening of nasolabial fold |
| A - ARM: Arm drift, unilateral weakness, heaviness, or numbness |
| S - SPEECH: Slurred speech (dysarthria), expressive or receptive aphasia |
| T - TIME: Time of Last Known Normal (LKN) -> Activate Stroke Code / 911! |
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Acute Emergency Diagnostics & Reperfusion Windows
- Emergent Non-Contrast Head CT: The immediate first-line imaging modality to definitively rule out intracranial hemorrhage prior to administering any thrombolytic or antithrombotic agent.
- Capillary Blood Glucose: Mandatory bedside test to exclude acute hypoglycemia (which can mimic acute focal stroke deficits!).
- Intravenous Thrombolysis (IV Alteplase [tPA] or Tenecteplase [TNK]):
- Window of Administration: Within $\le 4.5\text{ hours}$ of Last Known Normal (LKN).
- Blood Pressure Requirement: Blood pressure must be lowered to $<185/110\text{ mmHg}$ before thrombolysis is initiated, and maintained $<180/105\text{ mmHg}$ for at least 24 hours post-thrombolysis (using IV labetalol or nicardipine).
- Major Absolute Contraindications: Active internal bleeding, history of previous intracranial hemorrhage, intracranial neoplasm or aneurysm, recent major surgery or head trauma ($<3\text{ months}$), severe uncontrolled hypertension despite IV antihypertensives, platelets $<100,000/\mu\text{L}$, or therapeutic anticoagulation with DOACs or warfarin with $\text{INR} > 1.7$.
- Endovascular Mechanical Thrombectomy (EVT):
- Indicated for acute ischemic stroke caused by Large Vessel Occlusion (LVO) in the anterior circulation (internal carotid artery or proximal MCA $M_1$ segment).
- Window: Up to 6 to 24 hours from LKN in patients selected by advanced neuroimaging (CT perfusion / MRI DWI showing salvageable ischemic penumbra vs infarcted core).
3. Vascular Stroke Syndromes & Neuroanatomical Localization
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| VASCULAR STROKE LOCALIZATION MATRIX |
| |
| VASCULAR TERRITORY ANATOMICAL STRUCTURES INVOLVED HALLMARK CLINICAL MANIFESTATIONS |
| --------------------------------------------------------------------------------------------------- |
| Middle Cerebral Motor/sensory cortex for face * Contralateral hemiparesis & hemisensory loss |
| Artery (MCA) and upper extremity; Broca's (FACE & ARM > Leg). |
| (Most Common CVA!) & Wernicke's areas (dominant); * Dominant (Left) Hemisphere: APHASIA |
| Parietal lobe (non-dominant). (Expressive Broca's or Receptive Wernicke's). |
| * Non-Dominant (Right) Hemisphere: HEMINEGLECT, |
| anosognosia, spatial disorientation. |
| * Contralateral homonymous hemianopia. |
| * Conjugate gaze deviation TOWARD side of lesion.|
| |
| Anterior Cerebral Motor/sensory cortex for lower * Contralateral hemiparesis & hemisensory loss |
| Artery (ACA) extremity (paracentral lobule); (LEG & FOOT > Arm/Face). |
| Frontal lobes (prefrontal cortex)* Abulia, apathy, psychomotor slowing, mutism. |
| * Urinary incontinence (frontal micturition ctr).|
| * Primitive reflexes (grasp, suck). |
| |
| Posterior Cerebral Occipital visual cortex; * Contralateral HOMONYMOUS HEMIANOPIA with |
| Artery (PCA) Splenium of corpus callosum; MACULAR SPARING (dual MCA supply to fovea). |
| Thalamus (thalamic branches). * Visual agnosia, prosopagnosia (face blindness).|
| * Thalamic Pain Syndrome (Dejerine-Roussy): |
| severe delayed contralateral burning pain. |
| |
| Vertebrobasilar / Brainstem (Pons, Medulla), * The "4 D's": Dizziness (vertigo), Diplopia, |
| Posterior Circulation nuclei (CN III - XII). * CROSSED DEFICITS: Ipsilateral cranial nerve |
| palsy + Contralateral hemiparesis/sensory loss.|
| * Cerebellar Ataxia, nystagmus, dysmetria. |
| * Locked-in Syndrome (Basilar artery occlusion). |
| * Lateral Medullary (Wallenberg) Syndrome (PICA):|
| ipsilateral Horner syndrome, loss of pain/temp |
| to face, contralateral pain/temp loss to body. |
| |
| Lacunar Syndromes Small penetrating branches to * Pure Motor Hemiparesis (posterior limb of |
| (Small Vessel) internal capsule, thalamus, internal capsule - most common lacunar type). |
| or pons. * Pure Sensory Stroke (VPL nucleus of thalamus). |
| * Ataxic Hemiparesis (corona radiata / pons). |
| * Clumsy Hand-Dysarthria Syndrome. |
| * CRUCIAL: CORTICAL SIGNS (aphasia, neglect, |
| visual field cuts) ARE ENTIRELY ABSENT! |
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4. Transient Ischemic Attack (TIA) & Secondary Prevention
Transient Ischemic Attack (TIA) is defined as a transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute tissue infarction on neuroimaging (DWI-MRI). Clinical symptoms typically resolve within 15 to 60 minutes.
The ABCD2 Risk Stratification Score
The ABCD2 score predicts the 2-day, 7-day, and 90-day risk of subsequent completed stroke following a TIA.
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| THE ABCD2 SCORING SYSTEM |
| |
| FACTOR POINTS |
| ----------------------------------------------------------------------- |
| A - AGE >= 60 years 1 point |
| B - BLOOD PRESSURE: SBP >= 140 mmHg OR DBP >= 90 mmHg 1 point |
| C - CLINICAL FEATURES: |
| - Unilateral weakness with or without speech impairment 2 points |
| - Speech impairment WITHOUT unilateral weakness 1 point |
| D - DURATION OF SYMPTOMS: |
| - >= 60 minutes 2 points |
| - 10 to 59 minutes 1 point |
| - < 10 minutes 0 points |
| D - DIABETES MELLITUS (documented history) 1 point |
| ----------------------------------------------------------------------- |
| TOTAL SCORE: 0 - 7 points |
| * Low Risk (0-3 points): 2-day stroke risk ~1.0% |
| * Moderate Risk (4-5 points): 2-day stroke risk ~4.1% |
| * High Risk (6-7 points): 2-day stroke risk ~8.1% (90-day risk up to 18%) |
| |
| CLINICAL RULE: ABCD2 SCORE >= 4 MANDATES IMMEDIATE HOSPITAL ADMISSION! |
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Comprehensive TIA Diagnostic Workup
- Brain MRI with Diffusion-Weighted Imaging (DWI): The most sensitive imaging modality to detect subclinical acute cytotoxic edema / micro-infarction.
- Vascular Imaging of Carotid & Vertebrobasilar Systems: Carotid Duplex Ultrasonography, CT Angiography (CTA), or MR Angiography (MRA) of neck and head.
- Cardiac Workup: 12-lead ECG, Transthoracic Echocardiogram (TTE with agitated saline bubble study to detect patent foramen ovale; TEE if aortic arch atheroma or left atrial appendage thrombus suspected), and extended outpatient cardiac rhythm monitoring (Holter monitor or 30-day patch) to detect occult paroxysmal atrial fibrillation.
Evidence-Based Secondary Stroke Prevention Protocols
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| GUIDELINE-DIRECTED SECONDARY STROKE PREVENTION |
| |
| CLINICAL INDICATION RECOMMENDED PHARMACOTHERAPY PROTOCOL CLINICAL TARGETS & RULES |
| --------------------------------------------------------------------------------------------------- |
| Non-Cardioembolic Stroke / DUAL ANTIPLATELET THERAPY (DAPT): DAPT initiated within 24 hours|
| High-Risk TIA (ABCD2 >= 4) * Aspirin 81 mg daily + Clopidogrel 75 mg and strictly stopped at |
| or Minor Stroke (NIHSS <= 3) daily (after 300-600mg loading dose) 21 to 30 days to avoid long- |
| for exactly 21 to 30 DAYS, term hemorrhagic bleeding |
| followed by MONOTHERAPY (Clopidogrel risks. |
| 75 mg daily or Aspirin 81 mg daily). |
| |
| Cardioembolic Stroke / TIA DIRECT ORAL ANTICOAGULANT (DOAC): DO NOT USE ANTIPLATELETS FOR |
| secondary to Atrial * Apixaban (5 mg BID), Rivaroxaban ATRIAL FIBRILLATION! DOACs are|
| Fibrillation / Flutter (20 mg daily), or Dabigatran (150 mg BID). superior to Warfarin with |
| * Warfarin (target INR 2.0-3.0) if significantly lower risk of |
| mechanical prosthetic heart valves. fatal intracranial hemorrhage.|
| |
| Atherosclerotic Ischemic HIGH-INTENSITY STATIN THERAPY: Absolute LDL-C target: |
| Stroke / TIA * Atorvastatin 80 mg daily OR < 70 mg/dL (or >= 50% LDL-C |
| * Rosuvastatin 40 mg daily. reduction from baseline). |
| |
| Hypertension Management * Thiazide diuretic (Chlorthalidone) + Target BP < 130/80 mmHg in |
| ACEi / ARB (e.g., Lisinopril). chronic phase. |
| |
| Severe Symptomatic Carotid CAROTID ENDARTERECTOMY (CEA): Perform within 14 days of |
| Artery Stenosis (70 - 99%) * Surgical excision of atheromatous plaque symptom onset. Carotid artery |
| (or Carotid Artery Stenting [CAS]). stenting for high surgical risk|
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5. Peripheral Neuropathies & Mononeuropathies
Peripheral neuropathies are broadly divided into polyneuropathies (diffuse, symmetric processes) and mononeuropathies (focal nerve compression or infarction).
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| PERIPHERAL NEUROPATHY ETIOLOGIC MATRIX |
| |
| 1. METABOLIC / ENDOCRINE: Diabetes Mellitus (most common), Hypothyroidism |
| 2. TOXIC / NUTRITIONAL: Chronic Ethanol abuse, Vitamin B12 deficiency |
| (subacute combined degeneration), Pyridoxine (B6) excess or deficiency |
| 3. INFECTIOUS: Lyme disease, HIV, Post-herpetic neuralgia, Hansen's disease|
| 4. MEDICATION-INDUCED: Chemotherapy (Platinum, Taxanes, Vinca alkaloids), |
| Isoniazid, Metronidazole, Amiodarone, Fluoroquinolones |
| 5. IMMUNE-MEDIATED: Guillain-Barré Syndrome (acute inflammatory demyelin- |
| ating polyneuropathy - ascending paralysis, albuminocytologic dissoc.) |
| 6. RENAL / SYSTEMIC: Uremic neuropathy (ESRD), Paraneoplastic syndromes |
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Diabetic Peripheral Neuropathy (DPN)
- Pathophysiology: Chronic hyperglycemia generates advanced glycation end-products (AGEs), sorbitol accumulation via the polyol pathway, and microvascular endoneurial ischemia, causing length-dependent axonal degeneration.
- Clinical Presentation: "Stocking-glove" distribution beginning in the distal toes and feet, progressing symmetrically up the lower extremities before involving the hands. Symptoms include burning paresthesias, lancinating shooting pain, allodynia, numbness, and progressive sensory ataxia.
- Annual Screening Protocol:
- 10-g Semmes-Weinstein Monofilament: Applied perpendicularly to 10 plantar sites until the monofilament buckles (loss of sensation indicates high ulceration risk).
- Vibration Perception: Tested at the great toe interphalangeal joint using a 128-Hz tuning fork (loss of vibration is the earliest sign of large-fiber sensory loss).
- Deep Tendon Reflexes: Diminished or absent Achilles (ankle jerk) reflexes.
- Evidence-Based Pharmacotherapy:
- First-Line Agents:
- Duloxetine: 60 mg PO daily (SNRI; highly effective; also manages comorbid depression).
- Pregabalin: 75–150 mg PO BID (Alpha-2-delta calcium channel ligand; rapid pain relief; caution for peripheral edema and sedation).
- Gabapentin: 300–1200 mg PO TID (titrated gradually; requires renal dose adjustment).
- Second-Line: Tricyclic Antidepressants (Amitriptyline, Nortriptyline; use with caution in older adults), Venlafaxine, Capsaicin 8% topical patch.
- Avoid: Opioids (lacks long-term efficacy, high dependency risk).
- First-Line Agents:
Vitamin B12 Deficiency & Subacute Combined Degeneration
- Pathology: Deficiency of cobalamin leads to accumulation of methylmalonic acid (MMA) and homocysteine, resulting in defective myelin synthesis.
- Anatomical Triad of Subacute Combined Degeneration (SCD):
- Dorsal (Posterior) Columns: Loss of vibration sense, proprioception, positive Romberg sign, and sensory ataxia.
- Lateral Corticospinal Tracts: Upper motor neuron signs—spastic paresis, hyperreflexia, extensor plantar response (positive Babinski sign).
- Peripheral Nerves: Sensorimotor axonal neuropathy with paresthesias and distal numbness.
- Crucial Diagnostic Pearl: Neurological damage from B12 deficiency can occur in the absence of anemia or macrocytosis! When serum B12 is borderline (200–400 pg/mL), always measure serum Methylmalonic Acid (MMA) and Homocysteine (both are markedly elevated in true B12 deficiency).
Mononeuropathies: Carpal Tunnel Syndrome & Bell's Palsy
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| FOCAL MONONEUROPATHY COMPARATIVE MATRIX |
| |
| DISORDER NERVE & ANATOMY CLINICAL PRESENTATION & EXAM MANAGEMENT STRATEGY |
| --------------------------------------------------------------------------------------------------- |
| Carpal Tunnel MEDIAN NERVE compressed * Nocturnal paresthesias/burning* Volar wrist splinting|
| Syndrome (CTS) under flexor retinaculum in thumb, index, middle, and in NEUTRAL position at|
| within carpal tunnel of radial half of ring finger. night (first-line!). |
| wrist. * Thenar muscle atrophy (late). * Glucocorticoid |
| * Provocative Tests: injection into canal.|
| - PHALEN'S: Flex wrists 90° x * Surgical carpal |
| 60s -> paresthesias reproduced tunnel release for|
| - TINEL'S: Percussion over refractory or thenar|
| volar carpal tunnel -> tingling atrophy cases. |
| - DURKAN'S: Direct compression |
| over carpal tunnel (most sens!) |
| |
| Bell's Palsy FACIAL NERVE (CN VII) * Sudden-onset UNILATERAL FACIAL * ORAL PREDNISONE |
| (Idiopathic Facial inflammation/edema at WEAKNESS developing over <48h. (60-80 mg daily x |
| Palsy) stylomastoid foramen * CANNOT WRINKLE FOREHEAD, 7-10 days) initiated |
| (associated with HSV-1 cannot close eye tightly within 72 HOURS! |
| reactivation). (lagophthalmos), flat nasolabial * EYE PROTECTION: |
| fold, drooping mouth corner. Artificial tears Q1H,|
| * Loss of taste anterior 2/3 lubricating ointment |
| tongue, hyperacusis (stapedius).& tape eye shut at |
| * FOREHEAD INVOLVEMENT IS night (prevents |
| PATHOGNOMONIC FOR LMN LESION! corneal ulceration!)|
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| BELL'S PALSY (LMN) vs. ACUTE ISCHEMIC STROKE (UMN) |
| |
| LOWER MOTOR NEURON (CN VII) - BELL'S PALSY: |
| - Entire ipsilateral hemi-face paralyzed: |
| [CANNOT WRINKLE FOREHEAD] + [CANNOT CLOSE EYE] + [MOUTH DROOP] |
| - Forehead is INVOLVED because final motor pathway is destroyed. |
| |
| UPPER MOTOR NEURON (CORTICAL) - ACUTE STROKE: |
| - Lower half of contralateral face paralyzed: |
| [FOREHEAD IS SPARED / CAN WRINKLE FOREHEAD] + [MOUTH DROOP] |
| - Forehead is SPARED due to BILATERAL CORTICOBULBAR INNERVATION to the |
| upper facial motor nucleus! |
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6. Movement Disorders: Parkinson's Disease vs. Essential Tremor
Parkinson's Disease (PD)
Parkinson's disease is a chronic, progressive neurodegenerative disorder pathologically characterized by the degeneration of dopaminergic neurons in the substantia nigra pars compacta and the intracellular accumulation of Lewy bodies composed of misfolded alpha-synuclein protein.
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| THE CARDINAL "TRAP" OF PARKINSON'S |
| |
| T - TREMOR: Resting tremor (4-6 Hz), classically "pill-rolling", |
| ASYMMETRICAL at onset; decreases with voluntary purposeful movement. |
| |
| R - RIGIDITY: Increased resistance to passive movement throughout range of|
| motion; "lead-pipe" or "cogwheel" rigidity (tremor superimposed). |
| |
| A - AKINESIA / BRADYKINESIA: Slowness of movement initiation and execution|
| - Decreased blink rate, "masked facies" (hypomimia) |
| - Soft hypophonic speech, micrographic handwriting (micrographia) |
| - Shuffling festinating gait with diminished arm swing and en bloc |
| turning (multiple small steps to turn 180°). |
| |
| P - POSTURAL INSTABILITY: Loss of postural reflexes (positive Pull Test), |
| propulsion/retropulsion, frequent falls (manifests in later stages). |
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Non-Motor Manifestations of Parkinson's Disease:
- REM Sleep Behavior Disorder (RBD): Dream enactment behavior (thrashing, punching during sleep), often predating motor symptoms by 10–15 years.
- Anosmia / Hyposmia: Loss of olfactory sense (earliest clinical marker).
- Autonomic Dysfunction: Chronic constipation, neurogenic orthostatic hypotension, urinary urgency, erectile dysfunction, seborrheic dermatitis.
- Neuropsychiatric: Depression, generalized anxiety, apathy, visual hallucinations, and Parkinson's Disease Dementia (PDD).
Evidence-Based Pharmacotherapy for Parkinson's Disease
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| PARKINSON'S DISEASE PHARMACOTHERAPY MATRIX |
| |
| DRUG CLASS MECHANISM & AGENTS CLINICAL INDICATIONS ADVERSE EFFECTS & PEARLS|
| --------------------------------------------------------------------------------------------------- |
| Dopamine Precursor LEVODOPA / CARBIDOPA GOLD-STANDARD, most potent Nausea, orthostatic |
| (Gold Standard) (Sinemet: 25/100 mg TID) symptomatic drug. Indicated hypotension, dizziness. |
| - Levodopa crosses BBB and for older adults (>=65 yrs) Long-term: MOTOR |
| converts to dopamine. or patients with significant FLUCTUATIONS ("wearing- |
| - Carbidopa blocks functional disability. off") and Dyskinesias. |
| peripheral DOPA Administer 30-60 min |
| decarboxylase (prevents before protein meals! |
| nausea/arrhythmias). |
| |
| Dopamine Agonists PRAMIPEXOLE, ROPINIROLE, First-line monotherapy in IMPULSE CONTROL |
| (Non-Ergot) ROTIGOTINE (transdermal) YOUNGER patients (<65 yrs) DISORDERS (gambling, |
| - Directly stimulate D2/D3 to delay levodopa-induced hypersexuality, binge |
| dopamine receptors. motor complications. eating, compulsive shop)|
| Sudden sleep attacks, |
| hallucinations, edema. |
| |
| COMT Inhibitors ENTACAPONE (200 mg with Used EXCLUSIVELY as an Turns urine benign |
| each Sinemet dose), adjunct to Levodopa to treat ORANGE-BROWN. Must be |
| OPICAPONE "WEARING-OFF" fluctuations. given WITH levodopa. |
| - Inhibits catechol-O- Extends levodopa half-life. |
| methyltransferase. |
| |
| MAO-B Inhibitors SELEGILINE, RASAGILINE, Mild early monotherapy or Insomnia (Selegiline |
| SAFINAMIDE adjunct. Blocks central metabolizes to ampheta- |
| - Inhibits monoamine dopamine breakdown. mine). Potential |
| oxidase type B. Serotonin Syndrome with |
| SSRIs/SNRIs. |
| |
| NMDA Antagonist / AMANTADINE (100 mg BID/TID) Specifically indicated to Livedo reticularis |
| Antiviral - Promotes dopamine release treat LEVODOPA-INDUCED (mottled purplish skin),|
| and blocks NMDA receptor. DYSKINESIAS (chorea/dystonia)peripheral edema, confu-|
| sion in older adults. |
| |
| Anticholinergics TRIHEXYPHENIDYL, BENZTROPINE Restricted to YOUNG patients STRICTLY CONTRAINDICATED|
| - Blocks central muscarinic (<65 yrs) with SEVERE IN OLDER ADULTS (BEERS |
| cholinergic excess. RESTING TREMOR. CRITERIA: severe memory |
| loss, delirium, urinary |
| retention, constipation)|
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Essential Tremor (ET) vs. Parkinsonian Tremor
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| ESSENTIAL TREMOR vs. PARKINSON'S TREMOR |
| |
| FEATURE ESSENTIAL TREMOR (ET) PARKINSON'S TREMOR |
| ----------------------------------------------------------------------- |
| Tremor Activation ACTION / POSTURAL tremor RESTING tremor |
| (occurs holding arms out, (occurs when limb is |
| writing, drinking cup) completely relaxed) |
| Frequency High frequency (8-12 Hz) Low frequency (4-6 Hz) |
| Symmetry Bilateral & symmetric Asymmetric at onset |
| Anatomical Sites Hands/arms, Head (titubation)Hands, legs, jaw, lips; |
| Voice ("shaky voice"); HEAD IS TYPICALLY SPARED |
| Legs are spared! |
| Family History Autosomal dominant (60%) Sporadic (>85-90%) |
| Alcohol Response TEMPORARILY IMPROVES with No significant relief |
| small amounts of ethanol |
| Bradykinesia/RigidityABSENT PRESENT (TRAP tetrad) |
| First-Line Therapy PROPRANOLOL (60-240 mg/d) CARBIDOPA-LEVODOPA or |
| OR PRIMIDONE (50-250 mg/d) Dopamine Agonists |
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7. Geriatric Considerations & Fall Risk Mitigation
- Neurogenic Orthostatic Hypotension (nOH): Common in Parkinson's disease and autonomic neuropathies. Defined as a drop in SBP $\ge 20\text{ mmHg}$ or DBP $\ge 10\text{ mmHg}$ within 3 minutes of standing without a compensatory rise in heart rate. Management: Increase dietary salt and fluids, waist-high compression stockings, abdominal binders, elevating head of bed 30 degrees, and pharmacotherapy with Fludrocortisone (mineralocorticoid), Midodrine (alpha-1 agonist), or Droxidopa (norepinephrine precursor).
- Psychosis & Visual Hallucinations in Parkinson's Disease: Often triggered by dopaminergic medications or underlying disease progression. Traditional antipsychotics (Haloperidol, Risperidone, Olanzapine) are strictly contraindicated because they block D2 receptors and cause severe, life-threatening motor deterioration. Preferred treatments:
- Pimavanserin: Selective 5-HT2A inverse agonist (FDA-approved specifically for Parkinson's disease psychosis; does not block dopamine receptors!).
- Quetiapine: Low dose (12.5–25 mg QHS; lowest D2 receptor affinity).
- Clozapine: Highly effective but requires mandatory REMS monitoring for agranulocytosis.
8. Board-Yield Summary & Clinical Pearls
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| ANCC AGPCNP CLINICAL EXAM PEARLS |
| |
| * Suspected Stroke -> Non-Contrast Head CT FIRST to exclude hemorrhage. |
| IV thrombolysis (Alteplase/Tenecteplase) within 4.5 hrs; BP MUST be |
| < 185/110 mmHg prior to infusion. |
| |
| * TIA with ABCD2 Score >= 4 -> ADMIT TO HOSPITAL. Initiate DAPT (Aspirin |
| + Clopidogrel) for 21 days + High-Intensity Atorvastatin 80 mg daily. |
| |
| * Bell's Palsy (LMN) -> Paralyzes ENTIRE half of face (CANNOT wrinkle |
| forehead). Stroke (UMN) -> SPARES THE FOREHEAD due to bilateral cortical|
| innervation. Treat Bell's palsy with Prednisone within 72 hrs + eye lube|
| |
| * Vitamin B12 Deficiency -> Causes Subacute Combined Degeneration: dorsal |
| columns (loss of proprioception/vibration) + lateral corticospinal |
| tracts (spasticity/Babinski). Can occur WITHOUT ANEMIA or macrocytosis! |
| |
| * Parkinson's Disease in elderly -> Carbidopa-Levodopa is FIRST-LINE. |
| Dopamine agonists (pramipexole) cause IMPULSE CONTROL DISORDERS. |
| Anticholinergics (trihexyphenidyl) are CONTRAINDICATED (Beers Criteria).|
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Test Your Knowledge
A 58-year-old male presents to the urgent care clinic with sudden-onset right-sided facial weakness that began 24 hours ago. On physical examination, he is unable to raise his right eyebrow or wrinkle his right forehead, has incomplete closure of his right eyelid (lagophthalmos), and exhibits flattening of the right nasolabial fold with sagging of the right corner of his mouth. Sensation to light touch on the face is normal. Cranial nerves III through VI and VIII through XII are intact. Motor strength in all four extremities is 5/5, deep tendon reflexes are 2+ throughout, and gait is normal. What is the AGPCNP's most accurate clinical assessment and initial management plan?
A
B
C
D
Test Your Knowledge
A 68-year-old male with a history of hypertension and type 2 diabetes mellitus is brought to the clinic by his wife 2 hours after experiencing sudden-onset right arm and right leg weakness accompanied by difficulty speaking. His wife timed the episode: the weakness and speech impairment lasted approximately 25 minutes and then resolved completely. His current vital signs: BP 158/92 mmHg, HR 78 bpm, RR 16 bpm, SpO2 98% on room air. Neurological exam reveals 5/5 strength bilaterally, fluent speech, intact cranial nerves, and normal gait. What is this patient's ABCD2 risk score, and what is the AGPCNP's most appropriate immediate clinical action?
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Test Your Knowledge
A 71-year-old female with a 5-year history of Parkinson's Disease currently managed with Carbidopa-Levodopa 25/100 mg orally three times daily presents to the primary care clinic for routine follow-up. She reports that over the past 3 months, her resting tremor, limb stiffness, and gait slowness consistently re-emerge approximately 45 to 60 minutes before her next scheduled dose is due. Once she takes her medication, her symptoms improve significantly within 30 minutes. She denies involuntary writhing movements (dyskinesias), confusion, or hallucinations. What is the most appropriate therapeutic adjustment for this patient's Parkinson's symptoms?
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