Neurological & Oncological Disorders – Exam Review

Cerebral Palsy (CP)

Pathophysiology

• Non-progressive motor‐neuron disorder caused by an early brain insult (antenatal, perinatal or post-natal up to ≈2 yr)
• Primarily affects movement and posture; cognition can be spared or co-implicated depending on lesion site
• Lesion → abnormal neuronal signaling, muscle tone imbalance, reflex persistence

Types & Hallmarks

• Spastic (≈70 – 80 %)
  • Hypertonia, hyperreflexia, scissoring gait, toe-walking
• Ataxic
  • Cerebellar damage → poor balance/coordination, wide-based staggering gait
• (Additional types mentioned in standard texts: dyskinetic, hypotonic, mixed – review if on slides)

Clinical Signs / Gait Cues

• Asymmetric crawling, hand preference < 18 mo, scissoring legs, equinus (tip-toe) stance
• Observe gait pattern on exam; recognition of spasticity vs ataxia is testable

Symptom Management Medications (focus = spasticity)

• Drug classes: centrally acting skeletal-muscle relaxants & antispastics
  • e.g.
  • Baclofen (oral, intrathecal pump)
  • Diazepam, Tizanidine
  • Dantrolene sodium (direct muscle)
• ATI occasionally lists brand names – know at least one per class

Epidemiology “Prevalence” Cue

• Male > female (slight predominance, but confirm exact slide figure)

Multiple Sclerosis (MS)

Pathophysiology

• Auto-immune demyelination of CNS neurons → conduction block & axonal loss
• Oligodendrocyte injury → plaques/sclerotic lesions
• MRI hallmark: multifocal periventricular white-matter plaques (T2/FLAIR hyperintense)

Clinical Phenotypes

• CIS – clinically isolated syndrome
  • Single demyelinating event; may convert to MS
• RRMS – relapsing–remitting
  • Discrete attacks with full/partial recovery; most common
• SPMS & PPMS etc. (know defining course if covered)

Early vs Late Manifestations

• Early: optic neuritis, Lhermitte’s sign, sensory paresthesias
• Late: spasticity, ataxia, bowel/bladder dysfunction, cognitive decline

Disease-Modifying Treatments (DMTs)

• Interferon-β, Glatiramer, Teriflunomide
• Monoclonal antibodies with common suffix “-mab” e.g. Ocrelizumab, Natalizumab
  • Question tip: suffix recognition analogous to “-pril” (ACEIs)

Hydrocephalus

Pathophysiology & Causes

• Imbalance of cerebrospinal-fluid (CSF) production vs absorption → ventricular dilation ↑ICP
• Congenital aqueductal stenosis, post-hemorrhagic blockage, meningitis scarring (three obvious vs three distractors in MCQ)

Infant Assessment Findings

• Rapidly enlarging head circumference, bulging anterior fontanelle, scalp vein distension
• Sun-setting eyes, high-pitched cry, poor feeding

Definitive Treatment

• Ventriculo-peritoneal (VP) shunt
  • Diverts CSF to peritoneal cavity
• Key Post-op Complication to monitor
  • Shunt infection or obstruction → recurrent ↑ICP (single high-yield answer)

Parkinson’s Disease (PD)

Risk Factors

• Age > 60, male, pesticide exposure, rural living, traumatic brain injury, family history (if on slide)

Pathophysiology

• Dopaminergic neuron loss in substantia nigra pars compacta → ↓ dopamine in basal ganglia
• Accumulation of α-synuclein Lewy bodies (abnormal protein mentioned in lecture)

Cardinal Motor Features ("Parkinsonian Stuff")

• Resting tremor (“pill-rolling”)
• Bradykinesia / hypokinesia
• Rigidity (cog-wheel)
• Postural instability; shuffling gait, en-bloc turning, freezing episodes

Diagnostic/Therapeutic Drug Clue

• Levodopa (with carbidopa) challenge improves symptoms → supports diagnosis when imaging is non-definitive (no pathognomonic test)

Lung Cancer

Most Common Category

• Non-small-cell lung cancer (NSCLC) ≈ 85 % vs small-cell 15 %

Early Signs/Sx

• Persistent cough, hemoptysis, dyspnea, chest pain, hoarseness

Environmental vs Non-Environmental Risk Factors

• Environmental: cigarette smoke (active/passive), radon, asbestos, silica, diesel exhaust
• Non-environmental: genetics, prior lung disease (COPD), dietary factors, family history

NSCLC Sub-types & Location

• Squamous-cell carcinoma → centrally located (near hilum & bronchi)
• Adenocarcinoma → peripheral lung fields
  • (Large-cell also peripheral if noted)

Colon Cancer (Colorectal)

Risk Factors

• Age > 50, familial polyposis, IBD, high-fat/low-fiber diet, smoking, alcohol, obesity, red-meat intake

Role of Pre-cancerous Polyps

• Adenomatous polyps undergo dysplasia → carcinoma sequence; early identification/removal reduces incidence

GI Bleed Complication

• Chronic occult bleeding → iron-deficiency anemia (testable late finding)

Specific Symptom Terminology

• Sensation of incomplete evacuation = Tenesmus (high-yield italicized word)

Symptoms of Metastatic Disease (Late)

• Weight loss, hepatomegaly, jaundice, ascites, pulmonary lesions (choose late/advanced option)

Brain Cancer

Primary vs Secondary

• Primary originates within CNS; secondary = metastasis from another organ (lung, breast, melanoma etc.)

Most Common Primary Brain Tumor

• Glioblastoma multiforme (high-grade astrocytoma) (unless slides specify meningioma; verify)

General Early Symptoms

• Headache (worse a.m.), seizures, focal neuro deficits, vomiting without nausea, papilledema

Leukemia

Pathophysiology Highlights

• Malignant clonal proliferation of immature blast cells in bone marrow → crowding out normal hematopoiesis
• Results in anemia, thrombocytopenia, neutropenia

Bone-Marrow Dynamics

• Hypercellularity with > 20\% blasts (AML/ALL diagnostic threshold)

Common Adult Leukemias

• AML, CLL are most prevalent in adults (if slides list CML/ALL, know age bias)

Symptoms & Non-Symptoms

• Fatigue, infections, bruising/bleeding, bone pain, night sweats
• Select option not classically linked (e.g., isolated joint deformity) as “NOT associated”

Diagnostic Test & Site

• Bone-marrow aspiration/biopsy (posterior iliac crest most common site)

Splenic Effect

• Splenomegaly due to leukemic infiltration & extramedullary hematopoiesis

Lymphoma (Hodgkin vs Non-Hodgkin)

Pathophysiology Basics

• Malignancy of lymphoid tissue; uncontrolled proliferation of lymphocytes (B ± T depending on type)

Hodgkin Lymphoma (HL)

• Predominantly B-cell origin
• Pathognomonic Reed–Sternberg cells
• Presents with contiguous nodal spread

Non-Hodgkin Lymphoma (NHL)

• B and/or T cell lineage; non-contiguous spread, extranodal disease common

“B-Symptoms” (Systemic Symptoms)

• Unexplained fever > 38 °C, drenching night sweats, unintentional weight loss > 10 %/6 mo
  • Present more in HL but can be in high-grade NHL

Lymphadenopathy Hot-Spots

• Cervical (neck), supraclavicular, axillary, inguinal – palpate during physical exam

Risk Factors

• Immunodeficiency, EBV, HIV, autoimmune disease, prior chemo/radiation, age extremes (if on slide)

Cancer Therapy Concepts

Targeted Therapy vs Traditional Chemotherapy

• Targeted therapy
  • Binds specific molecular targets (e.g., EGFR, CD20)
  • Greater tumor selectivity, fewer off-target toxicities
• Chemotherapy
  • Non-selective, attacks rapidly dividing cells (DNA synthesis/mitosis)
  • Higher systemic toxicity (myelosuppression, alopecia, mucositis)

Quick Study Strategy Tips from Instructor

• Pay special attention to slide elements in parentheses, italics, or bold
• Use gait/appearance clues to identify CP subtype quickly
• Memorize suffix for MS DMTs (“-mab”)
• For hydrocephalus & VP shunt, remember single key complication (infection/obstruction)
• Contrast environmental vs non-environmental lung-cancer risks
• Recognize tenesmus as colon-cancer symptom word
• Know that levodopa response helps diagnose Parkinson’s when imaging inconclusive
• Remember splenomegaly linkage in leukemia
• Understand difference between targeted therapies and chemo for potential treatment-mechanism question

High-Yield Equation / Numeric Data

(No specific formulas in lecture; remember diagnostic blast threshold >20\% for acute leukemias)