Neurological Flashcards
Cranial nerve
1. Olfactory- sensory- smell
2. Optic- sensory- vision
3. Oculomotor- motor- most eye movement
4. Trochlear- motor- moves eye to look at nose
5. Trigeminal- both- face sensation, mastication
6. Abducens- motor- abduct eyes
7. Facial- both- facial expression, taste
8. Vestibulocochlear - sensory- hearing balance
9. Glossopharyngeal- both- taste, gag reflex
10. Vegas – both- gag reflex, parasympathetic innervation
11. spinal accessory- motor- shoulder shrug
12. Hypoglossal- motor- swallowing speech
0h, oh, oh , to , touch, and ,feel, very, good, velvet, such, heaven
some, say, marry, money, but, my, brother, says, big, brains matter ,more
TRANSIENT ISCHEMIC ATTACK (TIA)
TIAs are periods of focal ischemic cerebral neurologic deficits lasting less than 24 hours without residual deficits. Almost 1/3 of people diagnosed with a CVA have a history of a TIA.
Etiology: Embolization is often a known cause. Cardiac embolic causes include, atrial fibrillation, mitral valve disease, infectious endocarditis, atrial myxoma, and thrombi complicating a myocardial infection. Atrial septal defects and patent foramen ovale allow emboli into the veins. In addition ulcerated plaques on major brain arteries can be a source of emboli. Ischemia also occurs in atherosclerosis, intracerebral hemorrhage, fibromuscular dysplasia, hypotension, and hematological disorders (i.e. sickle cell disease, polycythemia, hyperviscosity syndromes).
TIA
Signs and symptoms-usually abrupt onset without warning and recover rapidly within a few minutes:
Altered vision-ipsilateral monocular blindness
Transient aphasia
Dysphagia
Parasthesias of contralateral arm, leg, or face
Sensory deficits
Dizziness
Nystagmus
Cognitive (confusion) or behavioral (dysarthria, weakness) abnormalities
Classification of TIA
Carotid - Secondary to carotid stenosis
Aphasia, dysarthria, change in LOC, weakness, numbness
Vertebrobasilar-Due to reduced blood flow from the vertebral arteries
Vertigo, ataxia, dizziness, visual field deficits, weakness, confusion
TIA
Laboratory and Diagnostic Findings
STAT CT scan when symptoms occur to identify possible cerebral hemorrhage or cerebral tumor
MRI brain is indicated to detect acute or subacute infarction. MRI is superior in detecting ischemic CVA
Carotid doppler to identify carotid stenosis
Echocardiogram to identify any cardiac emboli
Cerebral angiography is the gold standard for investigating integrity of the cervical or cerebral vasculature
Order CBC, fasting blood glucose, serum cholesterol, and homocysteine, EKG, Chest Xray
TIA
Differential Diagnosis
Focal seizure
Migraine
Hypoglycemia
ABCD2 Score for TIA
ABCD2 is used to assess for stroke risk after TIA or the recurrence of TIA. The score is optimized to predict the risk of stroke within 2 days after a TIA, but also predict stroke risk within 90 days.
Risk factors include:
- age greater than 60 is 1 point
- blood pressure systolic blood pressure greater than 140 or diastolic blood pressure greater than 90 is 1 point
- clinical features of TIA- unilateral weakness with or without speech impairment is 2 point
speech impairment without unilateral weakness is 1 point
duration
TIA duration greater than 60 minutes is 2 point
TIA duration 10-59 minutes is 1 point
diabetes is 1 point
A Score of 0-3 hospital observation may be unnecessary without another indication such as atrial fibrillation
a score of 4-5- hospital observation justified and most situation
a score of 6-7 hospital observation worthwhile
4 or higher is suggested to be the threshold for hospital admission.
Parkinson Disease A neurodegenerative disorder, which is the result of insufficient amounts of dopamine in the body. Patients often have a resting tremor, rigidity, and a slowness when moving.
Etiology: Parkinson’s rarely occurs on familial basis. Most commonly it is idiopathic. It may result form a mutations of several genes specifically, the LRRK2 and PARK 1 genes. Exposure to toxins and CO2 may result in the diagnosis. Occurs slightly more often among men than women. Onset is usually between 45 and 65 years of age.
SIGNS AND SYMPTOMS
1. Classic triad: resting tremor (commonly in the extremity), rigidity (arms, legs, neck stiffness with restricted range of motion), and Bradykinesia (slow movements in a deliberate manner)
- Postural instability
- Pull test- steps backward to recover from a slight tug form behind
- Falls-develop later in the disease process
- Gait: diminished arm swing, shuffling steps, bent forward posture, frozen gait (gets stuck while ambulating)
- Depression
- Dementia
- Anxiety
- Psychosis
- Apathy
- Sleep disturbance
- Disinhibition
- Urinary incontinence
- Sexual dysfunction
- Constipation
- Orthostatic hypotension
- Masked facial expression: immobile face, staring eyes with mouth slightly open
- Dysphagia
- Dysarthria
- Increased saliva
- Decreased blinking-
Myerson’s sign: repetitive tapping over the bridge of nose induce a sustained blink response - Absent or decreased sense of smell….What cranial nerve controls smell??????–OLFACTORY
Parkinson Disease LAb and diagnostic
There are no labs/diagnostic studies specific to Parkinson’s.
Diagnosis is based on history and physical exam findings.
CT scan and MRI are usually normal in Parkinson’s but may provide differential diagnosis
The Unified Parkinson’s Disease Rating Scale, provide a standard evaluation and measure of the disease and its progression.
What cranial nerves are responsible for ptosis and decreased uvula movement
CN VII, facial
CN IX, hypoglossal - voice swallow, tongue movement
CN X, palate rise
The treatment of acute MS flares, and a prevention of flares, include
Methyl prednisolone
Interferon
Glatiramer
Multiple sclerosis common assessment findings include
Weakness and lower extremities urinary retention and Lhermitte sign
Myasthenia gravis, common assessment findings include
Weakness starting in the facial muscles, proximal asymmetric, weakness, increase, fatigue, bulbar symptoms, diplopia, apoptosis, dysarthria, and dysphasia. No sensory changes.
Myasthenia gravis causes
Auto immune disorder, resulting in the reduction of the number of acetylcholine receptor sites at the neuromuscular junction
Disorder of the immune system
Characterized by weakness that may fluctuate after prolonged muscle use
Weakness is typical worse after exercise and better after rest
Variable clinical course with remissions and exacerbations
Multiple sclerosis cause
Auto immune disease marked by numbness weakness, loss of muscle, coordination, and problems with vision, speech, and bladder control
The bodies immune system attacks, Milan, a key substance that serves as a nerve insulator and helps in the transmission of nerve signals
Variable clinical course with remissions and exacerbations
Demyelinating disease of the central nervous system
An acquired immunemediated disease characterized by relapses and remission
Myasthenia gravis incidence
Affects 2 to 5,000,000 people in the United States per year
Predominate age 20 to 40 years, but may occur at any age
Incidence peaks in the third decade for females in the fifth and six decades for male
Occurs more commonly in women
Multiple sclerosis incidence
Greatest incidents in young adults, usually between 20 and 50 years of age
Most common in persons of western European descent, living in temperate zones particularly in northern Europeans, such as Scandinavian more prevalent in Caucasian
MS patients life expectancy decreases 5 to 7 years
Myasthenia gravis signs and symptoms
A ptosis, diplopia, dysarthria, dysphasia, extremity weakness, fatigue, respiratory, difficulty, sensory modalities, and deep tendon reflexes are normal
Multiple sclerosis signs and symptoms
Weakness, numbness, tingling, or an steadiness in a limb, may progressed all limbs
Spastic paraparesis
Diplopia, disk equilibrium, urinary urgency, or hesitancy, optic atrophy, nystagmus
Myasthenia, gravis, labs and diagnostics
Antibodies to acetylcholine receptors, AchR – ab, are found in the serum in about 85% of patients
MuSK antibodies present in 50% of patients that test negative for AChR
Thyroid function test, I found to be higher with more prevalence of thyroid disease
Vitamin B-12 may be low
ANA and RA factors are present
LP is normal
Multiple sclerosis, labs and diagnostics
Definitive diagnosis can never be based solely on laboratory findings
Mild lymphocytosis common
LP- Slightly elevated protein in CSF
Elevated CSF IgG
MRI of the brain
Myasthenia gravis management
No specific protocol, neurology referral
Anti-cholinesterase drugs that block, the hydrolysis of acetylcholine and are used for symptomatic improvement. Such as pyridostigmine bromide
Immunosuppressants
Plasmapheresis
Ventilator support may be needed during a crisis
Multiple sclerosis
No treatment to prevent progression of the disease, neurology referral
Recovery from acute, relapses hasten by steroids
Anti-spasmodic
Interferon therapy
Immunosuppressive therapy
Plasmapheresis
Myasthenic Crisis: respiratory failure, medical emergency that occurs in up to 20% of patients and requires intubation. The oropharyngeal and laryngeal muscles are weak resulting in airway obstruction. Worsening muscle weakness and diplopia are often seen prior to crisis. Patients with muscle-specific kinase (MuSK) antibody positive are more likely to go into crisis.
Precipitating factors: infection, stress, withdrawal of cholinesterase inhibitors, rapid introduction increase or taper of steroids, exposure to drugs (Neuromuscular Blocking agents, antibiotics like Macrolides, Aminoglycosides, and Fluoroquinolones, cardiac agents like Beta Blockers, Calcium Channel Blockers, Procainamides, quinidine, iodine contrast, quinine, chemotherapy agents)
Multiple Sclerosis
Relapsing-remitting (RR-MS)- clear and defined episodes of relapses and recovery. There is an interval of months or years after initial episode before new symptoms develop. There is no clinical progression between relapse episodes.
Secondary progressive (SP-MS)- usually initiates with RR-MS, followed by deterioration and progression of the disease. Patients usually do not return to baseline after relapsing episode
Primary progressive (PP-MS)- continued disease progression from initial episode. Some plateaus and minor temporary improvement. Most common in patients >40.
SEIZURES
Definition: A transient disturbance of cerebral function secondary to abnormal electrical activity in the brain.
Etiology
Often unknown
Metabolic disorders: acidosis, electrolyte imbalance, hypoglycemia, hypoxia, alcohol withdrawal
CNS infection
Head trauma
Tumors, other lesions
Vascular disease
Alzheimer’s disease
Most common cause is noncompliance with medication for epilepsy
CLASSIFICATION OF SEIZURES
Focal seizure without cognitive changes
Consciousness preserved
Jacksonian movements-convulsive jerking or parasthesias/tingling that spreads to different parts of the limb or body
Toddy’s paralysis: localized paresis in the involved region lasting minutes to hours
Sensory symptoms: flashing lights, simple hallucinations, alterations in taste, olfactory changes, paresthesias, buzzing
Autonomic symptoms: abnormal epigastric symptoms, pallor, sweating, flushing, pupillary dilation, piloerection
Speech arrest or vocalization
Nausea
May have an aura
Psychic symptoms: déjà vu, dreamy states, fear, distortion of time perception
Focal seizure with cognitive changes
Most common seizure in epileptics
Impairment in consciousness
Automatisms: lip smacking, chewing, swallowing, sucking, picking at clothes
May begin with a stare at the time consciousness is impaired
Frequently begin with an aura
Generalized seizures
Typical absence seizure
Sudden loss of consciousness (5-30 seconds), with eyes fluttering or muscle spasms, begins and ends quickly
Common in children 6-14
Frequently occur several times a day, often when the patient is quietly sitting
If the seizure occurs during conversation, the patient may miss a few words
Generalized seizures
Atypical absence seizure
Longer loss of consciousness
Motor signs
Less responsive to anticonvulsants
Generalized seizures
Generalized tonic-clonic seizures
Begins abruptly
Loss of consciousness or fall will occur
Respiratory arrest
Tonic (muscle rigidity) then clonic (synchronous muscle jerks) contractions of the muscles of the extremities, torso, and head
Urinary or bowel incontinence
Lasts 2-5 minutes
May bite tongue or lips
Postictal state: deep sleep, headache, amnesia of events, muscle soreness, nausea, confusion
Generalized seizures
Status epilepticus -
Series of seizures lasting longer than 5 minutes with the patient never returning to baseline between seizures
Medical emergency, requires immediate intervention
Most uncommon but most life threatening
The longer the seizure last, the more difficult it is to control
Seizures
LABORATORY AND DIAGNOSTIC FINDINGS
NP should obtain a thorough history from the patient and family or observers of the event
24 hour continuous EEG is used for diagnosis of epilepsy.
It is the most important test in determining seizure classification.
A normal EEG does not rule out a seizure.
CT Scan or MRI performed for all new-onset seizures
MRI preferred over CT scan to identify specific lesions
Lumbar puncture to assess for infectious process after CT or MRI has been used to rule out mass
CBC
Glucose, liver and renal function test
VDRL
Chemistry to assess any electrolyte imbalance
Magnesium and Calcium
ANA
ESR
ABG
Urinalysis, drug screen
Serum prolactin rises 2-3 times above normal for about 1 hour after >75% of tonic-clonic seizures
Seizures
DIFFERENTIAL DIAGNOSIS
Syncope
Cardiac disease
Brainstem ischemia
Psychogenic nonepileptic seizure
Seizures
TREATMENT
Supportive care
Maintain open airway
Protect patient from injury
Administer O2 if needed
Do not place anything in patient mouth
IV NS
EKG, monitor RR and BP
Benzodiazepines: Valium
Lorazepam
Phenytoin
Fosphenytoin
Phenobarbital-if not responsive to phenytoin
Barbiturate coma or general anesthesia with neuromuscular blockade
Monitor serum drug levels (i.e. Dilantin level)
Monitor liver function with valproic acid, carbamazepine, or felbate
Monitor CBC with carbamazepine, ethosuximide, or felbate
Medication dosages should be titrated to adequate serum levels
If the patient is seizure free, monitor the patient not the levels
Discontinuance of anti-epileptics should be gradual and never abruptly withdrawn
Vagus nerve stimulation is used in conjunction with medication in patients with severe uncontrolled seizures.
VAGAL NERVE STIMULATOR
MENINGITIS
Infection of the membranes of the pia mater (membrane surrounding the brain ) and arachnoid mater (above the Pia Mater) of the brain or spinal cord, caused by viral, bacterial, or fungal infections.
Acute bacterial meningitis is a medical emergency.
Meningitis should be a differential diagnosis in any patient with fever and neurologic symptoms, particularly if there is a history of recent infection.
ETIOLOGY
More than >80% of cases are caused by Streptococcus pneumonia, Hemophilus influenza, or Neisseria meningitides.
Predisposing factors include mastoiditis, trauma, pneumonia, sinusitis, otitis media, and congenital malformations.
SIGNS AND SYMPTOMS
Fever (>101)
Severe headache
Nausea
Vomiting
Nuchal rigidity “stiff neck” with flexion
Positive Kernig’s sign: Pain and spasm of the hamstring muscles
Positive Brudzinski’s sign: Legs flex at both hips and knees in response to flexion of the head and neck to the chest.
Seizures
Photophobia
Chills
Myalgias
Altered mental status
Assess all cranial nerves and for Babinksi reflex
Meningitis
LABORATORY/DIAGNOSTIC FINDINGS
Lumbar puncture should be completed ASAP
CSF will be cloudy or xanthochromic (yellow in color) with
Elevated pressure (>180 mmH2O), Elevated protein,
Decreased glucose,
Presence of WBCs
CT scan of the head is indicated before LP
Obtain blood and sputum cultures
Assess CBC, Chemistry (electrolytes),
Coagulation,
liver/renal panel
Chest and sinus films may be necessary to assess for infection
HIV/AIDs testing
Meningitis
TREATMENT
Control symptoms and maintain electrolyte balance
Consult infectious disease
Initiate antibiotic therapy ASAP (Vancomycin, Penicillin G, 3rd generation cephalosporin, fluoroquinolones)
Why is bacterial meningitis a medical emergency? may result in death or brain damage . Rapid progression
Why should the NP start antibiotics ASAP? Helps to reduce complications. give with steriods to help reduce rate of hearing loss or other complicaiton
