Neuro Flashcards
Parkinson’s Disease
A progressive, degenerative neurologic movement disorder
Potential factors:
Genetics
free radical stress
viral infection (postencephalitic syndrome)
environmental factors (carbon monoxide poisoning, s.e. of dopamine receptor blocking antipsychotics
Decreased levels of dopamine due to destruction of pigmented neuronal cells of the substantia nigra in the basal ganglia
Substantia nigra
Located in Midbrain
helps “smooth” out body movements
Clinical symptoms do not appear until 60% of the neurons have disappeared
Clinical Manifestations of Parkinson’s Disease
*Tremor- resting, pill-rolling
*Rigidity
*Bradykinesia- abnormally slow movement
Dementia, depression, sleep disturbances and hallucinations
Excessive sweating, paroxysmal flushing, orthostatic hypotension
Mask-like facial expression
Dysarthria: slowed speech
dysphagia
Meningitis
Infection or inflammation of the meninges covering the brain and spinal cord.
Bacterial meningitis is usually secondary to another infection:
Pneumonia
Sinusitis or mastoiditis
Otitis Media
- fever, headache, vomiting
- positive Meningeal signs (stiff neck)/Nuchal rigidity/Photophobia
- Positive Brudzinski and Kernig’s Sign
Brudzinski’s Sign (Meningitis)
Appearance of involuntary flexing of knees and hips with passive flexion of patient’s head.
Kernig’s Sign (Meningitis)
Positive when the leg is fully flexed at hip & knee at 90 ̊, and subsequent extension in the knee elicits pain & possible spasm of the hamstring.
Bacterial Meningitis
Cloudy, purulent CSF Increased opening pressure ↑ polymorphonuclear neutrophils (PMN) ↑ ↑ protein ↓ glucose Patient isolation
Viral/Aseptic Meningitis
Clear Normal/slightly elevated ↑ lymphocytes Moderately elevated protein Normal glucose No patient isolation
Myasthenia Gravis Clinical Manifestations
Muscle weakness Fatigue Ptosis Diplopia: double vision Difficulty chewing/swallowing Difficulty w/ speech (weakness of lower face) Symptoms worse as day progresses Myasthenic crisis: compromise on respiratory muscles
Myasthenia Gravis
Neuromuscular disorder affecting impulse transmission between motor neuron & muscle cell
Women > Men @ age <40 y.o.
Autoimmune
Antibody-mediated loss of Ach receptors in NMJ
Initiating factor?? Thymoma or thymus hyperplasia??
Multiple Sclerosis
Idiopathic
Slow-acting viral infection; autoimmune response of the nervous system in genetically susceptible individuals
Common in WOMEN ages 20-45/Northern European descent
Sensitized T cells will enter the brain and promote antibody production that damages the myelin sheath of the CNS
Plaques of sclerotic tissues appear on the demyelinated axons interrupting the neuronal transmission
The most common areas affected are
Optic & oculomotor nerves
Clinical Manifestations of Multiple Sclerosis
Visual problems such as diplopia, blurred vision, loss of visual field, and nystagmus
Sensory impairment, i.e. paresthesia
Emotional lability, i.e. mood swings, depression
Motor dysfunction
Fatigue
Muscle weakness & spasticity
Urinary problems
Guillian-Barre’ Syndrome (GBS)
An auto-immune attack of the peripheral nerve myelin
Acute, rapid segmental demyelination of peripheral nerves and some cranial nerves
Process is reversible (unlike MS)
Cell-mediated immune attack to the myelin sheath of the peripheral nerves Infectious agent (influenza-like) may elicit antibody production that can also destroy the myelin sheath
Clinical Manifestations of GBS
Sensory & motor impairments due to impairment of dorsal nerve roots (sensory) and ventral nerve roots (motor)
Ascending, symmetrical weakness and paralysis
diminished reflexes of the lower extremities
paresthesias
potential RESPIRATORY FAILURE (1/3rd of patients)
If ANS involvement:
Postural HOTN, arrhythmias, abnormal sweating, urinary retention
Alzheimer’s Disease Clinical Manifestations
Loss of short term memory (w/denial) Disorientation Impaired abstract thinking Apraxia: inability to use objects (pen to write) Difficulty learning Deterioration in personal hygiene Inability to concentrate Sundowner’s syndrome: at night, confusion/wandering in patients
Clinical Manifestations of a TIA
Dizziness Momentary confusion Difficulty with speech Visual disturbances Weakness of paralysis on one side of the body Ptosis Tinnitus
CVA Risk Factors
Paralysis or weakness in the face, arms and/or legs Confusion Personality changes Sudden change in eyesight Decreased motor skills Severe headaches
Ischemic CVA
Caused by occlusion of an artery supplying blood to the brain
Ischemic CVA will be localized to the area of occlusion
Two types:
thrombus - progressive occlusion (ischemic attacks)
embolus - sudden occlusion
Hemmoraghic CVA
Caused by a rupture in a cerebral artery
Ruptured artery causes inflammation of brain tissue
increased intracranial pressure
damage to both cerebral hemispheres
Because of widespread damage, often fatal
This type of CVA occurs suddenly
Results from arteriosclerosis or severe hypertension (most commonly), but also ruptured AVM, coagulopathies, drugs
S/S of CVA
Hemiplegia
one-half of a patient’s body is paralyzed
Hemiparesis
weakness on one side of the body
Dysarthria
poor articulation during speech…”slurred speech”
Dyspraxia
loss of the ability to coordinate and perform certain purposeful movements and gestures
Dysphagia
difficulty in swallowing
Subarachnoid Hemorrhage
Sudden/severe Headache…”the worst headache in my life” (vasospasms) Vomiting Loss of consciousness Signs of meningeal irritation Visual disturbances
Epidural Hematoma
Usually resulting from arterial tear
initial loss of consciousness, followed by a lucid interval
then rapid deterioration
headache, dilated pupil on affected side (ipsilateral), contralateral hemiparesis
surgical emergency
Subdural Hematoma
Between dura & arachnoid can manifest slowly (tear in small bridging veins) confusion, lethargy, headache ipsilateral pupil dilation seizures
Basal Skull Fracture Manifestations
CSF leakage Rhinorrhea, otorrhea Battle’s sign Ecchymosis over mastoid process area Raccoon eyes bilateral periorbital ecchymosis
Expressive vs. Receptive (Wernicke’s) Aphasia
Receptive aphasia, also known as Wernicke’s aphasia, is a type of aphasia in which an individual is unable to understand language in its written or spoken form.
Broca’s area: which governs language production
Expressive or Nonfluent
Wernicke’s area: which governs the interpretation of language.
Receptive or fluent
