Key Neurological Disorders

Why This Matters

Neurological disorders aren't just a list of symptoms to memorize—they're windows into how the brain actually works. When you study Alzheimer's, you're learning about memory consolidation. When you examine Parkinson's, you're seeing the dopamine system in action. Every disorder on this list reveals something fundamental about neural communication, brain structure, neurotransmitter function, or the relationship between genes and behavior. That's exactly what you're being tested on.

On exams, you'll need to connect specific disorders to their underlying mechanisms. Why does damage to the substantia nigra cause movement problems? How does demyelination disrupt neural signaling? Don't just memorize that "Alzheimer's causes memory loss"—know why amyloid plaques and tau tangles lead to cognitive decline, and how that connects to what you've learned about synaptic function and neural plasticity.

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Neurodegenerative Disorders: Progressive Neural Loss

These disorders share a common theme: the gradual death of specific neuron populations, leading to progressive decline in function. What makes each unique is which neurons die and where.

Alzheimer's Disease

• Amyloid plaques and tau tangles—these protein accumulations disrupt synaptic communication and trigger neuron death, primarily in the hippocampus and cortex
• Progressive memory loss begins with recent memories because the hippocampus (essential for forming new memories) is affected earliest
• Acetylcholine deficits result from damage to cholinergic neurons, which is why cholinesterase inhibitors are a common treatment approach

Parkinson's Disease

• Dopamine-producing neurons in the substantia nigra degenerate, disrupting the basal ganglia circuit that controls voluntary movement
• Motor symptoms—tremors, rigidity, and bradykinesia (slowness of movement)—reflect the loss of dopamine's role in initiating and smoothing movement
• Non-motor symptoms including depression and sleep disturbances often appear years before motor signs, suggesting widespread neural involvement

Huntington's Disease

• HTT gene mutation causes production of abnormal huntingtin protein, leading to neuron death in the striatum and cortex
• Autosomal dominant inheritance means a 50% chance of passing the mutation to offspring—a key example of single-gene neurological disorders
• Chorea (involuntary, dance-like movements) results from damage to inhibitory pathways in the basal ganglia, causing uncontrolled motor output

Amyotrophic Lateral Sclerosis (ALS)

• Motor neurons in the brain and spinal cord progressively die, causing muscle weakness, atrophy, and eventual paralysis
• Cognitive function typically preserved—this distinguishes ALS from other neurodegenerative disorders and highlights the specificity of neural vulnerability
• Both upper and lower motor neurons are affected, producing a combination of spasticity and muscle wasting

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Disorders of Neural Communication: Signaling Gone Wrong

These conditions demonstrate what happens when the transmission of neural signals is disrupted—whether through demyelination, abnormal electrical activity, or neurotransmitter imbalances.

Multiple Sclerosis

• Demyelination of nerve fibers—the immune system attacks myelin sheaths in the CNS, slowing or blocking action potential conduction
• Unpredictable relapses and remissions reflect the immune system's fluctuating activity and the brain's attempts at remyelination
• Diverse symptoms (vision problems, fatigue, motor dysfunction) depend on which neural pathways lose their myelin coating

Epilepsy

• Abnormal synchronous electrical activity in the brain causes seizures—essentially, too many neurons firing together when they shouldn't
• Seizure types vary based on where abnormal activity originates and how far it spreads (focal vs. generalized)
• Excitation-inhibition imbalance—often involves disrupted GABA (inhibitory) or glutamate (excitatory) signaling, a key concept in neural regulation

Schizophrenia

• Dopamine hypothesis—excess dopamine activity in mesolimbic pathways contributes to positive symptoms like hallucinations and delusions
• Positive symptoms (hallucinations, delusions) vs. negative symptoms (flat affect, social withdrawal) may involve different neural circuits
• Prefrontal cortex dysfunction contributes to cognitive symptoms and disorganized thinking, linking to executive function concepts

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Vascular and Acute Disorders: Sudden Disruption

Unlike progressive disorders, these conditions involve rapid onset due to interrupted blood flow or other acute events.

Stroke

• Ischemic strokes (blockage) account for ~87% of cases; hemorrhagic strokes (bleeding) are less common but often more severe
• Time-critical treatment—"time is brain" because neurons begin dying within minutes of oxygen deprivation
• Localized damage produces symptoms that map onto affected brain regions—left hemisphere strokes often cause language deficits; right hemisphere strokes may cause spatial neglect

Migraine

• Cortical spreading depression—a wave of neuronal depolarization followed by suppression may underlie migraine aura
• Trigeminovascular system activation causes the characteristic throbbing pain through inflammation of blood vessels and meninges
• Neurotransmitter involvement—serotonin, CGRP (calcitonin gene-related peptide), and other signaling molecules are therapeutic targets

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Neurodevelopmental Disorders: Altered Brain Development

These conditions emerge during brain development and reflect differences in how neural circuits form and function rather than degeneration of existing structures.

Autism Spectrum Disorders

• Spectrum presentation—symptoms range from mild social difficulties to significant communication and behavioral challenges, reflecting variable neural differences
• Altered connectivity patterns—research suggests differences in both local and long-range neural connections, affecting information integration
• Early brain overgrowth in some cases, followed by atypical pruning, points to disrupted developmental processes during critical periods

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Quick Reference Table

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Self-Check Questions

1. Both Parkinson's disease and Huntington's disease affect the basal ganglia. How do their movement symptoms differ, and what does this reveal about the different roles of dopamine vs. the striatum in motor control?

2. If a patient presents with memory problems, how would you distinguish early Alzheimer's disease from the cognitive effects of a stroke based on symptom onset and progression?

3. Multiple sclerosis and ALS both cause motor dysfunction. What is the key mechanistic difference between demyelination and motor neuron death, and how would symptoms differ?

4. Compare the dopamine hypothesis of schizophrenia with the dopamine deficit in Parkinson's disease. Why might increasing dopamine help one condition but worsen the other?

5. An FRQ asks you to explain how studying neurological disorders helps us understand normal brain function. Using two disorders from this guide, explain what each reveals about a specific brain structure or neurotransmitter system.