Chapter 34_2 flashcards
(21 cards)
Epilepsy: Pathophysiology (Epileptogenesis)
The transformation of a normal neuronal region into a chronically hyperexcitable area. It involves an imbalance between excitatory and inhibitory impulses, leading to high-frequency, synchronized firing of neurons.
Seizure Types: Focal vs. Generalized
Focal Onset: Arises from and is localized to one cerebral hemisphere. The person may be aware or have impaired awareness. Symptoms relate to the brain area affected (e.g., motor twitch in one hand). Generalized Onset: Begins in one hemisphere and rapidly spreads to involve both. Often involves loss of consciousness and tonic-clonic muscle movements.
Seizure First Aid: Key Safety Measures
The most important goal is to protect the patient from injury. Move objects away, do not restrain the person, and do not put anything in their mouth. Afterward, place the person on their left side to prevent aspiration.
Status Epilepticus: Definition & Treatment
A medical emergency defined as a continuous seizure lasting longer than 5 minutes, or more than one seizure within a 5-minute period without returning to a normal level of consciousness. First-line treatment is a benzodiazepine (e.g., lorazepam).
Tension-Type Headache (TTH): Characteristics
Most common primary headache. Described as bilateral, “band-like” pressure of mild to moderate intensity. Not worsened by physical activity.
Migraine Headache: Pathophysiology & Stages
A neurovascular headache involving trigeminal nerve activation and inflammation of cranial blood vessels. Four stages: Prodrome (neural hyperexcitability), Aura (cortical spreading depression), Pain (trigeminovascular activation), and Postdrome.
Migraine Headache: Classic Symptoms & Treatment
Symptoms: Severe, throbbing, often unilateral headache accompanied by nausea, vomiting, photophobia (light sensitivity), and phonophobia (sound sensitivity). Treatment: Acute attacks are treated with triptans (serotonin agonists) or NSAIDs. Preventive therapy may include beta-blockers or CGRP antagonists.
Cluster Headache (a type of TAC): Characteristics
Excruciating, unilateral, orbital, or supraorbital pain that occurs in clusters. Accompanied by prominent cranial parasympathetic signs on the same side, such as eye tearing/redness, rhinorrhea, and sweating.
Parkinson’s Disease: Core Pathophysiology
A progressive loss of dopamine-producing cells in the substantia nigra (part of the basal ganglia). The resulting dopamine deficiency creates an imbalance with acetylcholine, leading to movement disorders.
Parkinson’s Disease: Classic Triad of Motor Symptoms (TRAP)
T: Tremor at rest (often a “pill-rolling” tremor). R: Rigidity (cogwheel stiffness). A: Akinesia or Bradykinesia (slowness or absence of movement). P: Postural instability (imbalance and shuffling gait).
Parkinson’s Disease: Treatment
The cornerstone of treatment is dopamine replacement therapy using Levodopa (a precursor to dopamine) combined with Carbidopa (which prevents peripheral breakdown of levodopa, allowing more to reach the brain).
Amyotrophic Lateral Sclerosis (ALS): Pathophysiology
Also known as Lou Gehrig’s disease, it is a progressive neurodegenerative disorder that destroys both upper and lower motor neurons, leading to muscle weakness, atrophy, and eventual paralysis.
ALS: Clinical Manifestations
Key feature is painless muscle weakness. Sensory and cognitive functions remain intact. The disease is fatal, typically from respiratory failure due to paralysis of the diaphragm.
Multiple Sclerosis (MS): Pathophysiology
An autoimmune, demyelinating disorder where T-cells attack the myelin sheath of motor and sensory neurons in the CNS. This leads to the formation of fibrotic scar tissue (plaques), which disrupts nerve impulse conduction.
MS: Clinical Manifestations
Characterized by a course of remissions and exacerbations. Common symptoms include weakness, numbness, tingling, balance problems, blurred vision (optic neuritis is a common initial sign), and profound fatigue.
MS: Diagnosis & Treatment
Diagnosis: Requires evidence of demyelinating lesions separated in space and time, confirmed by MRI. Treatment: Immunomodulating agents (e.g., interferon, monoclonal antibodies) are used to reduce inflammatory attacks and slow disease progression.
Huntington’s Disease (HD): Pathophysiology
An autosomal-dominant genetic disorder caused by a mutation on chromosome 4, leading to an abnormal huntingtin protein that causes progressive neurodegeneration, particularly in the basal ganglia and cortex.
Huntington’s Disease (HD): Clinical Manifestations
The three main features are: 1. Involuntary motor symptoms (chorea - dancelike movements; athetosis - twisting movements). 2. Emotional and behavioral symptoms (depression, irritability). 3. Cognitive symptoms (dementia).
Guillain-Barré Syndrome (GBS): Pathophysiology
An acute, post-infectious peripheral neuropathy where an autoimmune response attacks the myelin of peripheral nerves. This results in ascending paralysis (weakness starting in the lower limbs and moving upward).
Myasthenia Gravis (MG): Pathophysiology
An autoimmune disease caused by autoantibodies that attack and destroy acetylcholine (ACh) receptors at the neuromuscular junction, preventing muscle contraction.
Myasthenia Gravis (MG): Cardinal Feature & Treatment
The cardinal feature is fluctuating, true muscle fatigue (not just tiredness) that worsens with repetitive motion and improves with rest. Ptosis (drooping eyelids) is often an early sign. Treatment: Acetylcholinesterase inhibitors (e.g., pyridostigmine) to increase the amount of ACh available at the synapse.
