Neuro

Question 1

Parkinson’s Disease

Answer 1

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

Question 2

Clinical Manifestations of Parkinson’s Disease

Answer 2

*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

Question 3

Meningitis

Answer 3

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

1. fever, headache, vomiting
2. positive Meningeal signs (stiff neck)/Nuchal rigidity/Photophobia
3. Positive Brudzinski and Kernig’s Sign

Question 4

Brudzinski’s Sign (Meningitis)

Answer 4

Appearance of involuntary flexing of knees and hips with passive flexion of patient’s head.

Question 5

Kernig’s Sign (Meningitis)

Answer 5

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.

Question 6

Bacterial Meningitis

Answer 6

Cloudy, purulent CSF 
Increased opening pressure 
↑ polymorphonuclear neutrophils (PMN)
↑ ↑ protein 
↓ glucose 
Patient isolation

Question 7

Viral/Aseptic Meningitis

Answer 7

Clear 
Normal/slightly elevated
↑ lymphocytes 
Moderately elevated protein 
Normal glucose 
No patient isolation

Question 8

Myasthenia Gravis Clinical Manifestations

Answer 8

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

Question 9

Myasthenia Gravis

Answer 9

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??

Question 10

Multiple Sclerosis

Answer 10

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

Question 11

Clinical Manifestations of Multiple Sclerosis

Answer 11

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

Question 12

Guillian-Barre’ Syndrome (GBS)

Answer 12

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

Question 13

Clinical Manifestations of GBS

Answer 13

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

Question 14

Alzheimer’s Disease Clinical Manifestations

Answer 14

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

Question 15

Clinical Manifestations of a TIA

Answer 15

Dizziness
Momentary confusion
Difficulty with speech
Visual disturbances
Weakness of paralysis on one side of the body
Ptosis
Tinnitus

Question 16

CVA Risk Factors

Answer 16

Paralysis or weakness in the face, arms and/or legs
Confusion
Personality changes
Sudden change in eyesight 
Decreased motor skills
Severe headaches

Question 17

Ischemic CVA

Answer 17

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

Question 18

Hemmoraghic CVA

Answer 18

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

Question 19

S/S of CVA

Answer 19

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

Question 20

Subarachnoid Hemorrhage

Answer 20

Sudden/severe Headache…”the worst headache in my life” (vasospasms)
Vomiting
Loss of consciousness
Signs of meningeal irritation
Visual disturbances

Question 21

Epidural Hematoma

Answer 21

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

Question 22

Subdural Hematoma

Answer 22

Between dura & arachnoid
can manifest slowly (tear in small bridging veins)
confusion, lethargy, headache
ipsilateral pupil dilation
seizures

Question 23

Basal Skull Fracture Manifestations

Answer 23

CSF leakage 
Rhinorrhea, otorrhea
Battle’s sign  
Ecchymosis over mastoid process area
Raccoon eyes 
bilateral periorbital ecchymosis

Question 24

Expressive vs. Receptive (Wernicke’s) Aphasia

Answer 24

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

Question 25

Paraplegia, Quadriplegia, Hemiplegia (Spinal Cord Trauma)

Answer 25

Paraplegia (leg paralysis)
Quadriplegia (multiple limbs)
Hemiplegia (one side of the body)

Question 26

Sympathetic Nervous System

Answer 26

Releases adrenergic catecholamines:
Epinephrine, norepinephrine, dopamine
Attach to adrenergic receptors
Think Fight or Flight!!!

Adrenergic Neurotransmitters are synthesized

Question 27

Parasympathetic Nervous System

Answer 27

Releases Cholinergic Acetylcholine
Attaches to cholinergic receptors
Think of chilling out!!!

Question 28

ICP (intracranial pressure)

Answer 28

Intracranial Contents:
80% brain tissue
10% blood
10% cerebrospinal fluid

Intracranial Pressure Rises as Brain+Blood+CSF volume Increases
There is only one way out of the intracranial vault –> the opening at the base of the skull known as the foramen magnum
When the brain is squeezed through the foramen magnum (herniation), the brainstem is compressed, the patient stops breathing, and the patient dies

Question 29

Battle’s sign

Answer 29

Ecchymosis over mastoid process area (bruise)

Question 30

Generalized Seizures

Answer 30

Absence Seizure (Petit mal)
common in children
Often very subtle
begins with a brief change in the LOC, indicated by automatisms (blinking, rolling of eyes and blank stares, lip smacking) or blank stare

Akinetic (Atonic) seizure
general loss of postural tone and a temporary loss of consciousness
AKA “drop attacks”

Question 31

Generalized Seizures

Answer 31

Myoclonic seizure
characterized by brief, involuntary muscular jerks of body extremities
General Tonic-Clonic seizure (Grand mal)
characterized by loss of consciousness and alternating movements of the extremities
Incontinence; possible cyanosis
Post-ictal (fatigue from aftermath) phase

Question 32

Partial Seizures

Answer 32

Simple partial seizure
typically limited to one cerebral hemisphere
Limited to one area of the body or to auditory, sensory or olfactory hallucinations
No impairment of consciousness

Complex partial seizure
begins with an aura
then with impaired consciousness 
purposeless behaviors like lip-smacking, chewing movements
Hallucinations
Post-ictal confusion

Question 33

Status Epilepticus

Answer 33

Continuous seizure state
Can occur during all types of seizures
Always considered a medical emergency, esp. tonic-clonic status

Question 34

Delerium vs. Dementia

Answer 34

Dementia develops over time, with a slow progression of cognitive decline. Delirium occurs abruptly, and symptoms can fluctuate during the day. The hallmark separating delirium from underlying dementia is inattention. The individual simply cannot focus on one idea or task.

Question 35

Brain Death

Answer 35

Brain death occurs when a person has an irreversible, catastrophic brain injury, which causes total cessation of all brain function (the upper brain structure and brain stem). Brain death is not a coma or persistent vegetative state. Brain death is determined in the hospital by one or more physicians not associated with a transplantation team.

Some causes of brain death include (but are not limited to):

Trauma to the brain (i.e. severe head injury caused by a motor vehicle crash, gunshot wound, fall or blow to the head)
Cerebrovascular injury (i.e. stroke or aneurysm)
Anoxia (i.e. drowning or heart attack when the patient is revived, but not before a lack or blood flow/oxygen to the brain has caused brain death)
Brain tumor