Neuro Disorders

Parkinsons Disease

progressive degenerative disorder that primarily affects dopaminergic neurons in the substantia nigra of the brain and impairs control of voluntary muscle movement

affects men slightly more often than women

Parkinsons Forms

primary → idiopathic with etiology or exact cause unknown, more common

secondary → caused factors like head trauma, stroke, brain tumor, infection, toxins, or dopamine blocking drugs (antipsychotics, antiemetics)

Parkinsons Diagnosis

most diagnosed between ages 60-70 with 15% diagnosed before age 50

diagnosis is clinical, based on history and neuro exams

no definitive lab tests, CT and MRI can rule our other conditions

Parkinsons Patho

degeneration of dopaminergic neurons in the substantia nigra pars compacta (in midbrain) → leads to dopamine deficiency in striatum

substantia nigra is part of the basal ganglia motor circuit → coordinates initiation and scaling of voluntary movement

lewy bodies form within affected neurons → abnormal protein aggregates (mostly a-synuclein) and contribute to neuronal dysfunction and death

microglia (CNS immune cells) are activated by lewy bodies → may cause chronic inflammation and worsen neuronal damage

Lewy Bodies

misfolded protein aggregates

activates microglia (macrophage like immune cells of the CNS)

Parkinsons Symptoms

resting tremors

bradykinesia

rigidity

postural dysfunction

Resting Tremor

asymmetric, rhythmic, low amplitude

unilateral → usually hands and feet

pill rolling → thumbs and fingers

disappears during sleep and worsens with anxiety and stress

intermittent → progressively worsens

Bradykinesia

slowness of voluntary movement

generalized slowness of movement

failure of antagonistic muscles to relax

loss of walking, blinking, swallowing saliva

Rigidity

involuntary contraction of striated muscle

stiffness of limbs and resistance of ROM

Postural Dysfunction

shuffling gait and balance problems

loss of postural reflexes → falls easily

stooped posture → leans to one side when seated

festinating gait → short and accelerated steps

Parkinsons Motor Symptoms

bradykinesia with fine motor impairment → slow and clumsy finger and hand movements

micrographia → small cramped handwriting

hypomimia → reduced facial expressions and mask-like appearance

speech changes → soft voice (hypophonia), monotone, slurred speech (dysarthria)

Parkinsons Facial Symptoms

low blinking → dry eyes, conjunctivitis, blepharospasm

drooling and dysphagia → difficulty managing saliva and swallowing

Parkinsons Autonomic Dysfunction

often earlier symptoms seen

constipation → due to early lewy body pathology in enteric nervous system

orthostatic hypotension → impaired sympathetic tone

urinary urgency/retention → disrupted autonomic control

diaphoresis → abnormal temperature and sweat regulation

Parkinsons Sexual Dysfunction

cognitive and neuropsychiatric symptoms

cognitive decline and dementia (usually in later stages)

sleep disturbances → including REM sleep behavior (can precede motor symptoms)

mood changes → depression, anxiety, apathy

Parkinsons Complications

impaired performance of activities of daily living → due to bradykinesia, tremor, and rigidity

fall related injuries → from postural instability and freezing of gat

aspiration risk → due to dysphagia and poor coordination of swallowing

UTIs → caused by autonomic dysfunction leading to urine retention

pressure ulcers → from decreased mobility and prolonged immobility

Parkinsons Meds

levodopa carbidopa → increases brain dopamine and carbidopa helps more drug reach the brain

anticholinergics → may reduce tremors, used in younger patients

delivery challenges → blood brain barrier limits which drugs can reach the brain

ultrasound can temporarily open the barrier to help deliver meds more effectively

Parkinsons Deep Brain Stimulation

electrodes are implanted in the brain to send signals that improve movement control

can reduce tremors, stiffness, and freezing when meds aren’t enough

Parkinsons Pallidotomy

rarely used

destroys a small brain area to reduce motor symptoms

Parkinsons Fetal Stem Cells

experimental implantation of dopamine producing cells into the brain

Parkinsons Therapies

physical therapy → improves balance, strength, and mobility

occupational therapy → helps with daily tasks and independence

speech therapy → improves voice, speech clarity, and swallowing

mental health support → addresses depression, anxiety, and cognitive changes

Parkinsons Nursing Care

patient and caregiver education → disease progression, med adherence, safety strategies

referral to support groups and exercise programs

ongoing assessment of chewing and swallowing (aspiration risk), mood and mental health, and nutritional status

home safety modifications to reduce fall risks

clothing adaptation → non skid velcro, slip on shirts, waistband pants

Seizures

sudden uncontrolled burst of electrical activity in the brain

triggers → missed meds, alcohol withdrawal, sleep deprivation, stress, flashing lights

most common in childhood and older age

Epilepsy

chronic conditions involving recurrent unprovoked seizures

Seizure Types

primary → no identifiable structural or metabolic cause

secondary → caused by structural or metabolic problems like brain tumors, stroke, brain injury, hyponatremia, or hypoglycemia

low Na → causes brains to swell and disrupt electrical signals

low glucose → deprives brain of energy needed to function

Seizure Diagnosis

clinical history → most important and includes onset, duration, symptoms, and recovery

EEG → detects abnormal electrical activity in the brain

MRI → identifies structural brain abnormalities like tremors, scarring, or stroke

serum chemistries evaluate for metabolic causes like low Na or low glucose

Epileptogenic Focus

groups of neurons becomes hyperexcitable and fire more easily than normal when stimulated

Seizure Patho

causes a 200% increase in metabolic demand for oxygen and nutrients → if demand is not met this can lead to brain damage

cause is imbalance between excitatory and inhibitory neurotransmitters → glutamate is excitatory and GABA is inhibitory

Focal Seizure

affects one cerebral hemisphere → partial

can spread and become generalized

Generalized Seizure

affects both hemispheres

Aura

type of focal aware seizure that may serve as a prodrome to a larger seizure

indicates that a larger seizure (usually generalized) may be imminent

often involves sensory symptoms such as a strange smell, visual change, or feeling of deja vu

not all seizures are preceded by this but any seizure can have one

Postictal State

occurs after a generalized seizure

characterized by a slow return to consciousness

person may be lethargic, confused, or even combative

common symptoms → confusion, headache, and fatigue

Focal Aware Seizure

begins in a specific area of one cerebral hemisphere

person remains awake and aware throughout the event