Neuro Flashcards

1
Q

What is the most potent agent that influences cerebral blood flow?

A

Carbon dioxide, Cerebral vessels dilate in response to CO2 levels greater than 45 mm Hg

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2
Q

GCS is a measure of?

A

consciousness and cognition and does not replace neurological assessment of specific brain function

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3
Q

GCS of 8 or less is consistent with?

A

Coma

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4
Q

What conditions limit the application of the GCS?

A

Medication, concurrent injuries-such as spinal cord injury

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5
Q

What is expressive dysphasia?

A

a deficit in language output or speech production from a dysfunction in the dominant frontal lobe. It varies from mild word-finding difficulty to complete loss of both verbal and written communication skills

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6
Q

What is receptive dysphasia?

A

The inability to comprehend language and follow commands

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7
Q

How can we assess short-term memory?

A

ask the patient to recall the names of three common words or objects (e.g., chair, clock, blue) after a 3-minute interval

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8
Q

How can we assess long-term memory?

A

by asking the patient questions about the distant past (e.g., birthplace, year of birth, year of graduation from school, year of marriage)

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9
Q

What is the most critical component of cranial nerve assessment?

A

Pupil examination… Normal pupil diameter ranges from 1.5 to 6 mm. Pupils are often assessed hourly for size, shape, equality, and direct and consensual response to light. Remember- Hypoxia and medications may also influence pupillary size and reactivity to light.

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10
Q

When do we use “arm drift”?

A

In a conscious patient, check for arm drift to detect subtle weakness. Ask the patient to close the eyes and stretch out the arms with palms up for 20 to 30 seconds. A downward drift of the arm or pronation of the palm indicates subtle weakness in the involved extremity

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11
Q

What is Flexor posturing?

A

involves rigid flexion and adduction of the arms, wrist flexion with clenched fists, and extension and internal rotation of the legs. It usually occurs secondary to damage of the corticospinal tract (also called decorticate).

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12
Q

What is Extensor posturing?

A

the result of a midbrain or pons lesion. In this posture, the arms and legs are rigidly extended, and the feet are in plantar extension (also called decerebrate)

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13
Q

What are some pathological reflexes that may reappear as a consequence of impaired neuro function?

A

Babinski reflex, the suck (sucking motions in response to touch the lips), snout (lip pursing in response to touching the lips), palmar (grasp in response to stroking the palm), and palmomental (contraction of the facial muscle in response to stimulation of the thenar eminence near the thumb) reflexes in adults

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14
Q

What causes increased intracranial pressure?

A

results when there is an increase of one of the three components comprising ICP: brain volume, blood, or CSF fluid. Normal range is 0-15mm Hg

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15
Q

When can herniation result?

A

When ICP is sustained at a pressure of 20 mm Hg for 5 minutes or longer, herniation may result

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16
Q

What can cause an increase in cerebral blood volume?

A

Loss of autoregulation, which provides a constant blood volume and cerebral perfusion pressure over a wide range of mean arterial pressures, can occur with head injury

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17
Q

What are some differences in a fluid-filled transducer system (used for Intracranial Pressure monitoring)?

A

(1) normal saline solution without preservatives must be used so as not to damage brain tissue, and (2) the flush system is not pressurized so that there is no possibility of flushing into the cranium

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18
Q

What is the priority management of a patient with increased intracranial pressure?

A

ensuring a patent airway. In addition to ensuring a patent airway, oxygenation must be supported. Previous practice of hyperventilation to decrease carbon dioxide, reducing the vasodilatory effect on cerebral blood vessels, has been abandoned because of the potential for ischemia

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19
Q

What kind of meds do we see given for increased intracranial pressure?

A

Osmotic and loop diuretics act to reduce brain tissue volume. Osmotic diuretics draw water from the extracellular space to decrease ICP. This effect occurs within minutes of administration. Loop diuretics remove sodium and water from injured brain cells. To sustain adequate cerebral perfusion pressure, fluid administration, guided by hemodynamic monitoring, must be optimized with the appropriate fluids. Sedation: Benzos, propofol, analgesics… induced hypothermia (Goal-34-35C), seizure prophylaxis, neuromuscular blockades

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20
Q

What is the blood pressure management for those with Increased ICP?

A

To maintain MAP 70-90mm Hg, CPP of at least 70 mm Hg, avoid hypertension (usually give Nicardipine) and avoid hypotension (give vasopressors)

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21
Q

What structures are included in a TBI usually?

A

injury can result in damage to the scalp, skull, meninges, and brain. An open injury involves a tear to the scalp or a fracture that extends into the sinuses. A closed traumatic brain injury occurs when there is no break in the scalp

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22
Q

Primary brain injury vs secondary brain injury:

A

Primary brain injury is direct injury to the brain tissue. As the brain is injured, it can sustain injury to the area under the direct impact (coup) as well as distal to the site of impact (contrecoup). Secondary brain injury occurs as a result of initial trauma and is characterized by cellular changes leading to vasogenic cerebral edema

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23
Q

Why is early recognition of a stroke needed?

A

to preserve blood flow to the brain and potentially reduce disability

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24
Q

What are the types of strokes?

A

Ischemic and Hemorrhagic. Types of hemorrhagic: intraparenchymal (uncontrolled hypertension), ruptured cerebral aneurysm (dilated cerebral artery that ruptures), arteriovenous malformation (congenital abnormality)

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25
Q

What are some tools used to assess an acute stroke?

A

History (time of onset of symptoms), neuro exam (mental status, cranial nerve function, motor strength, sensory function, neglect, coordination), NIH stroke scale; ABCs

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26
Q

What are some differences noticed in hemorrhagic stroke neuro assessment?

A

Localized headache, Nuchal rigidity, Pain above and behind the eye, Photophobia, Restlessness/irritability, Worst headache

27
Q

What are some differences in management for hemorrhagic strokes vs ischemic strokes?

A

Hemorrhagic Stroke- Goal: MAP < 130 mm Hg, “Glycemic management, Diagnostic exams, CT evaluation, Laboratory tests”, Medications: IV antihypertensives, Manage ICP-Osmotic diuretics. Ischemic Stroke- Goal: BP < 220 mm Hg; diastolic < 120 mm Hg, “”, Medications: rT-PA

28
Q

What is status epilepticus?

A

Seizures in close proximity to each other, Lasting longer than 30 minutes, Two or more without full recovery. Respiratory, neurological, and cardiac system assessments are the priority during status epilepticus. The first-line medication is a benzodiazepine, usually IV lorazepam (Ativan). If lorazepam fails to stop seizure activity within 10 minutes, or if intermittent seizures persist for longer than 20 minutes, levetiracetam (Keppra), phenytoin (Dilantin), fosphenytoin (Cerebyx), lamotrigine (Lamictal) or lacosamide (Vimpat) may be administered. Phenytoin is mixed only with normal saline and is stable in solution for up to 4 hours. Phenobarbital may be used as an additional medication to control SE, but its utility in SE is lessened by the length of time required to achieve a therapeutic effect

29
Q

What type of meningitis is a neuro emergency?

A

Bacterial… Bacteria gain access in one of three ways: (1) via the blood or through the spread of nearby infection, such as sinusitis; (2) by CSF contamination through surgical procedures or catheters; or (3) through the skull. Airborne droplets can be passed from infected individuals through sneezing, coughing, or kissing, and droplets can be passed through saliva and transmitted via drinks, cigarettes, or utensils

30
Q

What are some clinical manifestations of bacterial meningitis?

A

Headache, Fever, Vomiting, Rash (Initial rash associated with meningitis may be macular but progresses to petechiae and purpura on the trunk and extremities), Nuchal rigidity (Kernig’s sign and Brudzinski’s sign)… #1 test-lumbar puncture

31
Q

What are some medical and nursing management tools we use for bacterial meningitis?

A

Antibiotics, Corticosteroids, Droplet precautions (Private room, Dim light), Monitor for increased ICP, Seizure precautions

32
Q

What are some examples of incomplete SCI lesions?

A

Anterior cord syndrome, Central cord syndrome, Brown-Séquard syndrome

33
Q

What is the FOUR score?

A

a clinical grading scale designed for use by medical professionals in the assessment of patients with impaired level of consciousness. “Full Outline of Unresponsiveness.” Assesses four domains of neurological function: eye responses, motor responses, brainstem reflexes, and breathing pattern

34
Q

What is the eye test done to test eye movement for unresponsive patients?

A

Dolls eye or caloric reflex. Here, reflex is suppressed in alert patients. To test - elevate the HOB by 30 degrees (to minimize intracranial pressure) and then the examiner rapidly rotates the head from side to side while observing the patient’s open eyes (don’t perform if suspected c-spine injury). A normal response occurs when the eyes automatically move in the direction opposite the rotation (i.e. the head is turned left, the eyes move to the right). A positive Dolls Eye is GOOD/normal. An abnormal response occurs when the eyes passively move in the same direction as the head rotation. A negative doll’s eye response may indicate severe brain damage or brain death

35
Q

How do we calculate the CPP (Cerebral perfusion pressure)?

A

MAP-ICP=CPP (So any factor that decreases MAP and/or increase ICP decreases CPP). Normal CPP is 60-100…shows an adequately perfused brain

36
Q

What is Cushing’s Triad?

A

Reflects brainstem’s final effort to maintain cerebral perfusion. Seen when there is an increase in ICP. The triad consists of a widening pulse pressure (rising systolic, declining diastolic), irregular respirations, and bradycardia

37
Q

When can Cerebral salt-wasting syndrome occur?

A

Endocrine condition featuring hyponatremia and dehydration due head injury or sometimes a brain tumor. Symptoms include Polyuria (over 2 liters in 24 hours), thirst, and salt craving (if on a ventilator will not have symptoms of thirst). Muscle cramps, vertigo, anxiety, tachycardia or bradycardia, Hypotension due to severe hypovolemia. Treatment includes:
Hydration with sodium chloride containing fluids (may cautiously be given hypertonic saline) , Mineralocorticoid (flurionef) , Hourly I&O, daily weight, Close monitoring of serum sodium levels

38
Q

Do those with linear fractures (basilar fractures) generally lose consciousness?

A

No. Require close observation for 4 hrs and bed rest for 24 hours

39
Q

Which post-surgical patients should avoid excessive head-up positioning?

A

Those that have undergone evacuation of subdural hematomas (to avoid re-bleeding)… also, those after lumbar surgery or lumbar punctures… they should be kept flat 6-8 hrs following surgery

40
Q

What is important to remember for transsphenodial approach in neuro surgeries?

A

the nose is packed and need good oral care-avoid brushing teeth or use of a straw. To keep incision clean frequent warm saline rinses

41
Q

What are some of the post-op complications we see?

A

Diabetes Insipidus is a frequent complication and should be suspected if hourly urine output is >200 ml/hour, is of a low urine specific gravity (<1.005) and is accompanied by an increased plasma osmolality and extreme thirst. Intracranial hemorrhage or edema, Obstructive hydrocephalus, Fluid and electrolyte imbalance (especially hyponatremia), Hypoglycemia, Hypoxemia, Sepsis; Seizures (can occur at any time but are most common within the first 7 days after surgery)

42
Q

What medication do we use for cerebral vasospasms (common with aneurysm or AVM bleed requiring surgery)?

A

The calcium channel blocker used for this condition is oral nimodipine (Nimotop)

43
Q

What are some secondary causes of hemorrhagic strokes?

A

include excessive anticoagulation, inappropriate use of thrombolytics (recombinant tissue plasminogen activator [rt-PA or Alteplase]), vasopressor medications, drug abuse (cocaine), and coagulopathies

44
Q

What is the acute stroke assessments seen in the ED?

A

includes an eyewitness description of symptoms, identification of the exact time at which symptoms started, and a neurological assessment (within 10 mintues of arrival). The neurological examination includes evaluation of mental status (LOC, arousal, orientation), cranial nerve function, motor strength, sensory function, neglect, coordination, and deep tendon reflexes. Assessment and stabilization of the airway, breathing, and circulation are a priority. Vital signs are monitored, usually every 15 minutes for the first 6 hours. BP elevations are common in these patients. Because reducing the BP can decrease blood flow and oxygenation to the ischemic brain tissue, a gradual 20% lowering of the hypertensive BP is recommended to prevent enlargement of the infarcted area and worsening of the neurological deficit. Door-to-admission time of 3 hours in all patients

45
Q

What is the goal for each stroke?

A

Ischemic-to keep the systolic BP at less than 220 mm Hg and the diastolic BP at less than 120 mm Hg; Goal is to limit brain injury and maximize recovery which requires rapid identification and intervention. In the case of embolic stroke that means that if qualifies IV fibrinolytic treatment is provided within 3 hours of onset of symptoms *Neurologic assessment and CT of head takes priority over ECG (should be done within 25 minutes of arrival) . In hemorrhagic stroke, the goal is a MAP less than 130 mm Hg. BP is managed carefully with IV medications such as labetalol, nitroprusside, or nicardipine. Rapid drops in BP can cause further neurological deterioration by decreasing cerebral perfusion and extending the area of cerebral ischemia. Because hyperglycemia may exacerbate the extent of neurological injury, glycemic control is advocated. Hyponatremia due to cerebral salt wasting may occur; sodium and fluid replacement are necessary to maintain a normal sodium level

46
Q

What are some differences seen in patients with SAH than those with ischemic strokes?

A

When arterial blood enters the subarachnoid space, its presence is irritating to the meninges. The patient may complain of a localized headache, stiff neck (nuchal rigidity), pain above and behind the eye, and photophobia. Patients with SAH are often anxious and agitated as a result of pain, altered LOC, and cognitive changes. If conscious, the patient may complain of “the worst headache of my life.”

47
Q

What are symptoms of a stroke?

A

Weakness or numbness of one side of the body (face, arm, leg, or any combination of these), Slurred speech or an inability to comprehend what is being said, Visual disturbance, such as transient loss of vision in one or both eyes, double vision, or a visual field deficit, Dizziness, incoordination, ataxia, or vertigo, Sudden-onset severe headache (“worst headache of my life”) and Vomiting (projectile) without nausea

48
Q

What is Autonomic Dysreflexia?

A

Occurs T6 or above after resolution of spinal shock, Intense sympathetic response to stimuli (Kinked urinary catheter, Fecal impaction)
Symptoms of Severe hypertension, headache, and bradycardia. Need to Assess and remove the cause, Elevate the HOB, give oxygen, may need antihypertensive medication

49
Q

What is Myasthemia Gravis?

A

A progressive neuromuscular disease of the lower motor neurons characterized by weakness and fatigue of the voluntary muscles, Defect in transmission of nerve impulses at the myoneural junction. Primarily affects women 20-30 years of age and in men 50-60 years of age. There may be insufficient secretion of acetylcholine and an excessive secretion of cholinesterase. Fatal outcomes often associated with respiratory due to aspiration. Positive Tensilon test- Also to differentiate between myasthenia crisis and cholinergic crisis

50
Q

What are the symptoms for Myasthemia Gravis?

A

Stress, menses, heat and illness can exacerbate symptoms, Fluctuating weakness & fatigue of commonly used voluntary muscles, Symptoms mild in the morning, worse later in day, Rest may temporarily improve symptoms, Facial and proximal limb weakness, head may bob up and down difficulty raising arms (can’t raise arms to brush hair), Masklike expression and weakness of face, Difficulty chewing, dysphagia, drooling, aspiration, Ptosis with incomplete eye closure and diplopia, Weak, hoarse voice, may fade to a whisper, Difficulty breathing with diminished breath sounds, Respiratory paralysis and failure, Stress incontinence and anal sphincter weakness

51
Q

What is the the medical management for MG?

A

Corticosteroids, Azathiprine/Imuran (auto immune), Cyclosporine (Sandimmune) and MyM (Cellcept) to prevent organ rejection originally, Plasmapheresis (only used in crisis states), and IV immunoglobin

52
Q

What are some signs of MG crisis?

A

Usually involves respiratory distress and failure, Tachypnea, increased weakness and fatigue, Anxiety, restlessness, irritability, Inability to chew, dysphagia, Elevated temperature, Speech impairment…If untreated may lead to cardiac arrest

53
Q

What are some symptoms of Cholinergic Crisis?

A

(overmedication of anticholinerase) Restlessness, Weakness and vertigo, Blurred vision, Dysphagia, Dyspnea and wheezing
Abdominal cramps, N&V, diarrhea, Muscle tremors, spasms or weakness, Sweating, lacrimation, excess oral secretion and salvation

54
Q

What med do we give in Cholinergic crisis?

A

Atropine

55
Q

What is trigeminal neuralgia?

A

aka tic douloureux, is a facial pain syndrome that may be recurrent or chronic. Characterized by unilateral facial pain following the sensory distribution of cranial nerve V, controlling sensation to the lower eyelid, cheek, nostril, upper lip, upper gums and some muscles of chewing. May be accompanied by facial spasms. Pain is stabbing and most often affects right side of face, pain thought to be associated with impaired inhibitory mechanisms in the brainstem caused by excessive firing of irritated fibers of trigeminal nerve

56
Q

What are some triggers of trigeminal neuralgia?

A

Chewing, talking, smiling, Drinking hot or cold fluids, Touching, shaving, brushing teeth blowing nose, and Cold air striking face

57
Q

What is some Treatment for Trigeminal neuralgia?

A

Adjunct treatments electrical and thermal simulation, Drug therapy with carbamazepine (Tegretol), gabapentin, Lyrica, or baclofen, Surgical treatment aimed at disrupting pain. The three operative procedures used are 1) gama knife surgery, microvascular decompression percutaneous stereotatic rhizotomy

58
Q

What is caused by compression of cranial nerve VII?

A

Bells Palsy, the muscles controlling expression on one side of the face are paralyzed

59
Q

What test is done if lyme disease is suspected (in bells palsy)?

A

ELISA test… CT scan if cranial nerve tumor is suspected

60
Q

What is some treatment for Bells palsy?

A

Lubricating eye drops and patching eye at night to prevent corneal abrasions, Analgesics for pain, Steroids early in the course of illness may help shorten duration, Antiviral drugs such as Aclocylovir are sometimes used if herpes virus suspected, Electrical stimulation of the facial nerve and physical therapy. In some cases hypoglossal-facial nerve anastomosis to restore partial facial function if none by 6-12 months

61
Q

What are some strategies to relieve symptoms of restless leg syndrome?

A

walking, stretching, moderate exercise, or a warm bath

62
Q

What are some meds for RLS?

A

Many of the drugs prescribed for RLS are also used for either Parkinson disease (PD) or epilepsy. Dopamine agonists such as pramipexole (Mirapex) and ropinirole (Requip) are oral drugs used extensively. Gabapentin enacarbil (Horizant) is an antiepileptic drug (AED) that is also approved by the U.S. Food and Drug Administration (FDA) for RLS

63
Q

What is Gullain-Barre Syndrome?

A

Demyelination of peripheral nerves and is a result of immune-mediated pathologic processes… symptoms include initial muscle weakness/pain, ascending paralysis, and autonomic dysfunction. Potential for respiratory and/or cardiovascular distress or failure due to thoracic muscle weakness and hypotension

64
Q

What is some treatment for GB?

A

Plasmaphersis… Plasma usually replaces itself, or patient is transfused with albumin. Need to improve mobility and prevent complications with PT/OT