Neurological & Oncological Disorders – Comprehensive Exam Review Notes

Cerebral Palsy (CP)

• Pathophysiology

  • Non-progressive lesion or malformation of the developing brain → permanent disorders of movement & posture.
  • Etiologies: prenatal hypoxia/ischemia, intra-uterine infections, prematurity with intraventricular hemorrhage, kernicterus, perinatal stroke.
  • Results in abnormal muscle tone, reflexes, coordination, and possible cognitive/ sensory impairments.

• Classification / Types

  • Spastic (≈ 70 – 80 %)
  • Upper-motor-neuron pattern: hypertonia, hyperreflexia, clonus.
  • Scissor gait, toe-walking, crouched posture.
  • Ataxic
  • Cerebellar involvement → impaired balance & depth perception, wide-based unsteady gait, intention tremor.
  • (Other types for reference: Dyskinetic/athetoid, Mixed)

• Clinical Presentation

  • Gait pattern in slides: scissor-like adduction of legs with toe walking (classic for spastic CP).
  • Delayed motor milestones, persistent primitive reflexes, seizures, speech & swallowing difficulties.

• Pharmacologic Symptom Management (focus = spasticity)

  • Classes: centrally acting skeletal-muscle relaxants, benzodiazepines, botulinum toxin, intrathecal baclofen.
  • Brand names highlighted by ATI (know at least one per class):
  • Baclofen (e.g., Lioresal) – intrathecal pump for severe cases.
  • Diazepam (Valium) – short-term relief; watch for sedation.
  • Dantrolene (Dantrium) – hepatotoxicity monitoring.
  • Botulinum toxin type A (Botox) – focal injections to selected muscles.

• Epidemiology

  • Higher prevalence in males than females (know gender distribution).

Multiple Sclerosis (MS)

• Pathophysiology

  • Immune-mediated demyelination of CNS white matter → axonal damage & plaque formation.
  • MRI hallmark: discrete sclerotic plaques (white matter lesions) in periventricular areas.

• Clinical Patterns

  • CIS (Clinically Isolated Syndrome) – first demyelinating episode < 24 h; may convert to MS.
  • Relapsing-Remitting (RRMS) – episodic neurologic deficits with full/partial recovery.
  • Others for reference: Secondary progressive, Primary progressive.
  • Know typical manifestations for each (e.g., optic neuritis in CIS; sensory/motor relapse in RRMS).

• Signs & Symptoms

  • Early: numbness/paresthesiae, optic neuritis (painful vision loss), Lhermitte sign.
  • Late: spasticity, ataxia, bowel/bladder dysfunction, cognitive decline.

• Disease-Modifying Therapies (DMTs)

  • Suffix clue stressed in lecture: most oral agents end in “-mab” (monoclonal antibodies) or “-mod/-imod” (sphingosine-1-P modulators).
  • Examples: Ocrelizumab, Natalizumab, Fingolimod.
  • Purpose: reduce relapse rate & new MRI lesions.

Hydrocephalus

• Pathophysiology

  • Imbalance between cerebrospinal fluid (CSF) production & absorption → ventricular dilation ↑ intracranial pressure (ICP).
  • Types: communicating vs non-communicating (obstructive).

• Common Causes (select obvious answers)

  • Aqueductal stenosis, intraventricular hemorrhage (preemies), meningitis scarring.
  • Eliminate unrelated distractors by understanding CSF pathway.

• Infant Assessment Findings

  • Rapidly enlarging head circumference, bulging anterior fontanelle, splayed cranial sutures, “sun-setting” eyes, poor feeding, irritability, high-pitched cry.

• Standard Treatment

  • Ventriculoperitoneal (VP) shunt (only one treatment option emphasized).
  • Major Nursing Concern: shunt malfunction/infection → monitor for fever, vomiting, lethargy, abdominal distention.

Parkinson’s Disease (PD)

• Risk Factors

  • Age > 60, male sex, rural living/pesticide exposure, traumatic brain injury, genetic variants (LRRK2, PARKN).

• Key Molecular Players

  • Protein accumulation: α-synuclein–containing Lewy bodies inside degenerating neurons.
  • Neurochemical deficit: dopamine loss in substantia nigra → impaired basal ganglia output.

• Cardinal Motor Features (TRAP)

  • Tremor at rest (pill-rolling).
  • Rigidity (cog-wheel).
  • Akinesia/bradykinesia (slowed initiation, shuffling gait).
  • Postural instability.

• Diagnostic/Therapeutic Role of Levodopa

  • Responsive improvement to carbidopa/levodopa supports clinical diagnosis because no definitive lab test exists.

Lung Cancer

• Most Common Category overall: Non-Small-Cell Lung Cancer (NSCLC) (~85 %).

  • Subtypes & Location
  • Squamous-cell carcinoma – central/hilar bronchus, cavitation.
  • Adenocarcinoma – peripheral lung fields, may arise in scars.

• Early Signs & Symptoms

  • Chronic cough, hemoptysis, chest pain, dyspnea, hoarseness.

• Environmental vs Non-Environmental Risk Factors

  • Environmental: cigarette smoke (active/passive), radon gas, asbestos, silica, diesel exhaust, air pollution.
  • Non-environmental: genetic predisposition (EGFR, ALK), prior radiation, underlying lung disease (COPD, pulmonary fibrosis).
  • Examination will ask to differentiate these lists.

Colon (Colorectal) Cancer

• Risk Factors

  • Age > 50, family history, hereditary polyposis (FAP, HNPCC), precancerous adenomatous polyps, IBD (UC > Crohn), high red-meat/low-fiber diet, obesity, smoking.

• Complication of Chronic GI Bleeding

  • Occult/lower GI bleed → iron-deficiency anemia (microcytic).

• Cardinal Symptom Term

  • Tenesmus – sensation of incomplete evacuation after defecation (highlighted on slide).

• Late / Metastatic Signs

  • Hepatomegaly, jaundice, ascites, weight loss, pulmonary nodules.

Brain Cancer

• Primary vs Secondary

  • Primary originates in brain parenchyma/meninges (e.g., gliomas, meningiomas).
  • Secondary (metastatic) arises from systemic tumors (lung, breast, melanoma) and spreads to brain.

• Most Common Primary Malignancy

  • Glioblastoma multiforme (grade IV astrocytoma).

• General Signs & Symptoms (often early & non-specific)

  • Headache (worse AM), seizures, nausea/vomiting, focal neurologic deficits, papilledema, cognitive/personality change.

Leukemia

• Pathophysiology

  • Malignant transformation & uncontrolled clonal proliferation of hematopoietic precursors in bone marrow → crowding out normal lineages.
  • Blast cells = immature precursors; their excessive release into blood impairs normal RBC/platelet production.

• Bone-Marrow Consequences

  • Anemia (↓ RBC), thrombocytopenia (↓ platelets), neutropenia (↓ functional WBC) → fatigue, bleeding, infections.
  • Splenomegaly due to sequestration & extramedullary hematopoiesis.

• Common Adult Types

  • Acute Myeloid Leukemia (AML), Chronic Lymphocytic Leukemia (CLL), Chronic Myeloid Leukemia (CML).

• Typical Symptoms vs Non-associated

  • Associated: fever, night sweats, pallor, petechiae, bone pain, recurrent infections.
  • Not associated: focal neurologic deficits (unless CNS leukemic spread), peripheral edema (unless CHF co-morbid).

• Key Diagnostic Test

  • Bone-marrow aspiration/biopsy with flow cytometry & cytogenetics.

Lymphoma

• Pathophysiology

  • Malignancy of lymphoid tissue (nodes, spleen, extranodal sites) derived from mature B, T, or NK cells.

• Hodgkin vs Non-Hodgkin

  • Hodgkin Lymphoma (HL)
  • Reed–Sternberg cells (B-cell origin).
  • Mostly B-cell lineage.
  • Presents with orderly contiguous node spread.
  • Non-Hodgkin Lymphoma (NHL)
  • Heterogeneous; B and T/NK cell variants.

• “B-Symptoms” (systemic constitutional symptoms)

  • Unexplained fever > 38 °C, drenching night sweats, unintentional weight loss > 10 % in 6 mo.

• Risk Factors

  • Immunosuppression (HIV, transplant), EBV, HTLV-1, autoimmune disease, pesticides.

• Common Sites of Lymphadenopathy

  • Cervical (neck), supraclavicular, axillary, inguinal, epitrochlear, mediastinal (seen on CXR).

Cancer Treatment Modalities

• Targeted Therapy vs Traditional Chemotherapy
  • Targeted therapy
  • Acts on specific molecular targets (receptors, enzymes) unique/over-expressed on cancer cells.
  • Examples: tyrosine-kinase inhibitors, monoclonal antibodies.
  • Spares most normal cells → fewer systemic toxicities; resistance can develop via mutation of target.
  • Chemotherapy
  • Non-specific cytotoxic agents that disrupt DNA replication or mitosis in rapidly dividing cells.
  • Causes broad adverse effects (myelosuppression, alopecia, mucositis).

Quick Reference: Organs Affected in Leukemia

• Spleen: congestive splenomegaly → early satiety, LUQ pain, cytopenia from sequestration.
• Liver: hepatomegaly.
• Bone: marrow expansion → bone pain.

Study Strategy Tips (per Instructor)

• Review every bullet point on lecture slides; pay attention to italicized/parenthetical text.
• Identify drug classes & brand names exactly as listed by ATI.
• For pattern questions, recall the instructor’s verbal “walk-throughs” that guide you to obvious eliminations.