CLINICAL CARE OF THE NERVOUS SYSTEM

Question 1

The Management of a Patient with a Headache

Overview

Answer 1

(1) One of the most common medical complaints
(2) 12 to 16% of the population in North America
(3) 150 million lost workdays to headache each year
(4) Many do not present to physician for evaluation
(5) Headaches can be caused by many other illnesses
(6) Of note, rarely due to refractive error (eyestrain) alone
(7) A thorough history and physical exam is of great importance

Question 2

THE MANAGEMENT OF A PATIENT WITH A HEADACHE

Differential Diagnosis/Danger Signs

Answer 2

(1) Sudden onset or “thunderclap” headache
(a) Could be a subarachnoid hemorrhage (SAH)
(2) Absence of prior headache/s similar to present one
(a) Could be CNS infection
(3) Focal neurologic signs other than auras
(a) Could be stroke or tumor
(4) Other physical symptoms like fevers
(a) Could be meningitis
(5) Rapid onset with exercise
(a) Could be intracranial hemorrhage associated with brain aneurysm
(6) Associated with nasal congestion
(a) Could be sinusitis
(7) Associated with papilledema
(a) Could be increased intracranial pressure

Question 3

THE MANAGEMENT OF A PATIENT WITH A HEADACHE

Reasons to refer for imaging

Answer 3

(1) Recent change in pattern, frequency, or severity of headaches
(2) Progressive worsening despite therapy
(3) Focal neurological deficits or scalp tenderness
(4) Onset of headache with exertion, cough, or sexual activity
(5) Visual changes, auras, or orbital bruits
(6) Onset of headache after age 40
(7) History of trauma, hypertension, fever

Question 4

TYPES OF HEADACHES
Tension Headaches
1. Overview and presentation
2. Diagnosis
3. Treatment

Answer 4

(a) Overview and presentation
1) Most prevalent headache
2) Bilateral headaches
3) Often occurs daily
4) Characterized as “vice-like” in nature
5) Often exacerbated by emotional stress, fatigue, noise, glare
6) May be associated with hypertonicity of neck muscles.
(b) Diagnosis
1) No diagnostic tests are required
(c) Treatment
1) NSAIDS
a) MOA: Inhibits cyclooxygenase, reducing prostaglandin and thromboxane synthesis.
b) Adverse Reactions: GI bleeding, MI, nephrotoxicity, hepatotoxicity, dyspepsia, rash, fluid retention.
c) Types of NSAID
(1 Ibuprofen (Motrin) 400- 800 mg PO q 4- 6 hours, Max 2400mg/24 hours
(2 Naproxen (Naprosyn) 250- 500 mg PO q12 hours
d) Tylenol
(1 Dose: 325-1000 mg PO q 4-6 hours, max 4 grams/24 hours
(2 MOA: Antipyretic effect via direct action on the hypothalamic heatregulating center, analgesic MOA unknown
(3 Adverse Reactions: Hepatotoxicity, anemia, thrombocytopenia, rash, nausea
(4 Contraindications: Hepatic or renal impairment, chronic alcohol abuse

Question 5

TYPES OF HEADACHES
Cluster Headaches
1. Overview and presentation
2. Diagnosis
3. Treatment

Answer 5

(a) Overview and presentation
1) Usually affects middle aged men but can also affect women
2) Intense unilateral pain that starts around the temple or eye
3) Patients is often restless and agitated due to the pain
4) Episodes often occur 15 minutes to 3 hours
5) Usually occur seasonally and attacks are grouped together
6) Other associated symptoms
a) Ipsilateral congestion or rhinorrhea
b) Lacrimation and redness of the eye
c) Horner syndrome (Ptosis, miosis, anhidrosis)
7) After resolution of attacks there is a hiatus of several months
(b) Treatment
1) Oral treatment during an attack is generally unsatisfactory
2) Inhaled 100% oxygen for 15 minutes is initial treatment of choice
3) Subcutaneous Sumatriptan (Imitrex) - Anti-migraine medication
a) Dose: SubQ Initial: 6 mg; may repeat if needed ≥1 hour after initial dose (maximum: 6 mg per dose; two 6 mg injections per 24-hour period)
b) MOA: Selective agonist for serotonin (5-HT1B and 5- HT1D receptors) on intracranial blood vessels and sensory nerves of the trigeminal system; causes vasoconstriction and reduces neurogenic inflammation.
c) Adverse Reactions: Tingling, dizziness/vertigo, feeling hot
d) Contraindications: Ischemic heart disease or signs or symptoms of ischemic heart disease (coronary artery vasospasm, Prinzmetal angina, angina pectoris, myocardial infarction, silent myocardial ischemia); history
of cerebrovascular syndromes (including strokes, transient ischemic attacks), history of hemiplegic or basilar migraine; peripheral vascular disease (including ischemic bowel disease); uncontrolled hypertension; use
within 24 hours of ergotamine derivatives; use within 24 hours of another
4) Oral Zolmitirptan (Zomig) – Oral anti-migraine medication if they are able to tolerate.
a) Dose: Initial: 2.5 mg, may repeat if needed ≥ 2 hour after initial dose
(maximum single dose: 10 mg per 24-hour period).
b) MOA: Selective agonist for serotonin (5-HT1B and 5-HT1D receptors) on intracranial blood vessels and sensory nerves of the trigeminal system; causes vasoconstriction and reduce neurogenic inflammation associated with antidromic neuronal transmission correlating with relief of migraine.
c) Adverse Reactions: Gastrointestinal unpleasant taste, chest pain, weakness, dizziness/vertigo, feeling hot.
d) Contraindications: Ischemic heart disease or signs or symptoms of ischemic heart disease (coronary artery vasospasm, Prinzmetal angina, angina pectoris, myocardial infarction, silent myocardial ischemia);
history of cerebrovascular syndromes (including strokes, transient ischemic attacks), history of hemiplegic or basilar migraine; peripheral vascular disease (including ischemic bowel disease); uncontrolled hypertension; use within 24 hours of ergotamine derivatives; use within
24 hours of another 5-HT1 agonist; concurrent administration or within 2 weeks of discontinuing an MAO type A inhibitors; Wolff-Parkinson- White syndrome or arrhythmias associated with other cardiac accessory conduction pathway disorders; severe hepatic impairment.

Question 6

TYPES OF HEADACHES
Migraines
1. Overview and presentation
2. Diagnosis
3. Treatment

Answer 6

(a) Overview and presentation
1) Gradual build-up of a throbbing headache, that may be unilateral or bilateral
2) Duration of several hours
3) Aura may or may not be present
a) Visual disturbances such as visual field deficits or visual hallucinations (stars, light slashes, zigzags, etc)
b) Other focal disturbances such as aphasia or numbness, tingling, clumsiness, or weakness in a circumscribed distribution
4) Family history often positive for headaches
5) May have associated nausea and vomiting
(b) Diagnosis
1) Made clinically by HPI
(c) Management
1) Avoidance of precipitating factors, together with prophylactic or symptomatic pharmacologic treatment if necessary.
2) During acute attacks - rest in a quiet, darkened room until symptoms subside.
3) Migraine Abortive Treatment
a) Simple analgesics/NSAIDS: Ibuprofen, Naprosyn, Aspirin, Acetaminophen, Ketorolac (Toradol) 30mg IV/IM once or every 6 hours or 60mg IM once (max 120mg/day)
b) Sumatriptan (Imitrex)
(1 Dosing: Oral: A single dose of 25 mg, 50 mg, or 100 mg (taken with fluids). If a satisfactory response has not been obtained at 2 hours, a second dose may be administered. Results from clinical trials show that
initial doses of 50 mg and 100 mg are more effective than doses of 25mg, and that 100 mg doses do not provide a greater effect than 50 mg and may have increased incidence of side effects OR SubQ: 6mg IM.
4) Zolmitriptan (Zomig)
a) Dose: Initial: 2.5 mg, may repeat if needed ≥ 2 hour after initial dose (maximum single dose: 10 mg per 24 hour period).
(d) Migraine Prophylaxis
1) Preventative treatment indicated when migraines occur more than 2-3 times per month or associated significant disability
2) Antihypertensives: Beta-blockers such as Propranolol, Metoprolol
a) Propranolol (Inderal)
b) Dosing: Oral two divided doses starting at 40 mg a day; dose range 40-160 mg daily
c) MOA: Nonselective beta- adrenergic blocker (class II antiarrhythmic); competitively blocks response to beta1- and beta2- adrenergic stimulation
d) Adverse Reaction: CHF, bradycardia, heart block, bronchospasm, hepatitis
e) Contraindications: Bradycardia, heart failure, hypotension, hepatic impairment
3) Antidepressants
a) Amitryptyline
(1 Dosing: Start at 10mg at bedtime; dose range 20-50mg at bedtime
(2 MOA: Tricyclic antidepressant
(3 Side effects: Drowsiness, dry mouth, constipation, tachycardia, palpitations, orthostatic hypotension, weight gain, blurred vision, urinary retention
4) Anticonvulsants:
a) Topiramate
(1 Dose: 100-200mg a day
(2 Side effects: Paresthesia, fatigue, anorexia, diarrhea, weight loss, and nausea
5) Treatment for concurring symptoms
a) Antiemetics: Promethazine (Phenergan) - 1st generation antihistamine, anti- nausea and vomiting medication
(1 Dosing: 12.5 to 25 mg PO/IM/IV/Rectal every 4-6 hours as needed
(2 MOA: Non-selectively antagonizes central and peripheral histamine H1 receptors; possesses anticholinergic properties, resulting in
antiemetic and sedative effects
(3 Adverse Reactions: Respiratory depression, seizures, hallucinations,
heat stroke, drowsiness, sedation, photosensitivity

Question 7

TYPES OF HEADACHES
Post Traumatic
1. Overview and presentation
2. Diagnosis
3. Treatment

Answer 7

a) Overview and presentation
1) After head injury, it is common to have headaches
2) Symptoms occur within 1-2 days of injury, and subside within 7-10 days
3) Often accompanied by impaired memory, poor concentration, emotional instability, and increased irritability
(b) Treatment
1) No special treatment required
2) Simple analgesics are appropriate first line therapy

Question 8

TYPES OF HEADACHES
Mediction Overuse Headaches
1. Overview and presentation
2. Diagnosis
3. Treatment

Answer 8

(a) Overview and presentation
1) Present in about 50% of patients with chronic daily headaches
2) Patients typically present with chronic pain or with complaints of headache unresponsive to medication
3) History will often reveal heavy use of analgesics
(b) Treatment
1) Treatment is to withdraw medications
a) Expect improvement in months, not days

Question 9

MANAGEMENT OF A PATIENT WITH SEIZURES

Epidemiology

Answer 9

(1) ~5-10% of the population will have at least one seizure
(2) Highest incidence occurring in early childhood and late adulthood
(3) Epilepsy is characterized by recurrent unprovoked seizures

Question 10

MANAGEMENT OF A PATIENT WITH SEIZURES

Pathophysiology

Answer 10

(1) An abnormal, excessive, hypersynchronous discharge from an aggregate of CNS neurons
(2) Can have various manifestations

Question 11

MANAGEMENT OF A PATIENT WITH SEIZURES

Etiology of seizure

Answer 11

(1) Young adults (18-35 years)
(a) Trauma
(b) Metabolic disorders (Alcohol withdrawal, uremia, hyper/hypoglycemia)
(c) CNS Infection
(2) Older adults (>35 years)
(a) Cerebrovascular disease
(b) Brain tumor
(c) Metabolic disorders
(d) Degenerative disorders (Alzheimer)
(e) CNS Infection

Question 12

MANAGEMENT OF A PATIENT WITH SEIZURES
Seizure Classification
Partial Seizures

2. Diagnosis
3. Management and Treatment

Answer 12

(a) Depends on how much cortical involvement occurs with seizure
(b) Preictal phase can have auras that are associated to onset of seizure
(c) Focal seizure with retained awareness
1) Formerly known as simple partial seizure
2) Only one part of the brain is affected
3) Presentation depends on focal area involved
a) For example: Seizure that begins in occipital cortex can lead to flashing lights sensation

(f) Postictal phase
1) Somnolence, confusion or headache that may occur for several hours
2) Patient often have no recollection of event
3) Weakness of limbs may occur (“Todd paralysis”)
(g) Diagnosis of seizure
1) Video EEG monitoring
(h) Management and treatment
1) First Aid
a) Clear the room, maintain the airway if needed
b) For partial seizures, redirect gently
c) Started IV catheters
d) Blood work
(1 Electrolytes, LFT, CBC
(2 Finger stick glucose
2) Treatment for active seizure
a) Diazepam 5 mg IV/IM Q5-10 minutes; do not exceed 30 mg
(1 MOA: Modulates postsynaptic effects of GABA
transmission leading to increase in presynaptic inhibition
(2 Side effects: Ataxia, hypotension, respiratory depression
b) MEDEVAC immediately
(i) Complications of seizure
1) Status eplilepticus (EMERGENCY)
a) Definition: Single seizure lasting more than or equal to 5 minutes or 2 or more seizure between which there is an incomplete recovery of consciousness
b) Treatment:
(1 Diazepam 5mg IV/IM Q5-10 minutes; do not exceed 30mg
(2 Valproic acid 30mg/kg
(3 Correct any underlying problem that may be contributing to seizure
(4 Intubation

Question 13

MANAGEMENT OF A PATIENT WITH SEIZURES
Partial Seizures
Focal Seizure with Impaires Awareness

Answer 13

(d) Focal seizure with impaired awareness
1) Formerly known as complex partial seizure
2) Only one part of the brain is affected
3) During seizure patient appears to be awake but not in contact with others in environment and do not respond normally to instruction or questions
4) Patients often have no memory of what occurred during the seizure
5) May exhibit automatisms
a) Facial grimacing
b) Gesturing
c) Lip smacking
d) Chewing
e) Repeating words or phrases

Question 14

MANAGEMENT OF A PATIENT WITH SEIZURES
Partial Seizure
Generalized Seizure

Answer 14

(e) Generalized seizures
1) Involves the entire brain
2) May or may not lead to alteration of consciousness
3) Most common type is the tonic-clonic seizure (AKA grand mal)
a) Tonic phase characterized by sudden muscle stiffening
b) Clonic phase characterized by rhythmic jerking
(1 Tongue biting is common in this phase
c) Episodes usually last 1-2 minutes
4) Other types
a) Absence seizure
b) Clonic seizure
c) Atonic seizure

Question 15

MANAGEMENT OF A PATIENT WITH SEIZURES

1

Answer 15

(f) Postictal phase
1) Somnolence, confusion or headache that may occur for several hours
2) Patient often have no recollection of event
3) Weakness of limbs may occur (“Todd paralysis”)
g) Diagnosis of seizure
1) Video EEG monitoring

Question 16

MANAGEMENT OF A PATIENT WITH SEIZURES

1.

Answer 16

2) Differences between epileptic seizure
a) PNES episodes usually last longer than 2 minutes
b) Patients eyes are closed during PNES events
c) Incontinence is less common in PNES
d) Usually there is no postictal phase in PNES
3) Diagnosis is made with video EEG (no changes in electrical activity)
4) Treatment
a) Psychotherapy with cognitive behavioral therapy or interpersonal therapy

Question 17

DETERMINE THE MANAGEMENT OF A PATIENT WITH STTROKE TO INCLUDE CVA AND TIA
Blood Supply of the Brain

Answer 17

(1) Internal Carotid Arteries
(a) Branch from common carotid artery
(b) Supplies the majority of the ipsilateral cerebral hemisphere
(c) Two major branches
1) Anterior cerebral artery (ACA)
2) Middle cerebral artery (MCA)
(2) Vertebral - Basilar Arteries
(a) Two vertebral arteries fuse to become the basilar artery
1) The Basilar artery then branches to become the right and left Posterior cerebral arteries (PCA)
(b) Supplies the Cerebellum and Brainstem
(3) Circle of Willis
(a) Interconnects the Internal Carotid and Vertebral Basilar Arteries
1) The PCA connects internal carotid artery and vertebral basilar arteries
2) The ACA connects the anterior cerebral arteries
3) The MCA is a direct branch off of the internal carotid artery

Question 18

DETERMINE THE MANAGEMENT OF A PATIENT WITH STTROKE TO INCLUDE CVA AND TIA
Definitions and classification of strokes

Answer 18

(1) Two types of stroke representing very opposite conditions
(2) The “stroke” is the acute neurologic injury that occurs as the result of the interrupted blood flow to the brain
(3) Hemorrhagic stroke: Rupture of a blood vessel causing bleeding into the brain and lack of cerebral blood flow leading to ischemia
(4) Ischemic stroke: Blockage of a blood vessel causing lack of cerebral blood flow leading to ischemia
(a) TIA and CVA are subtypes of ischemic stroke

Question 19

DETERMINE THE MANAGEMENT OF A PATIENT WITH STTROKE TO INCLUDE CVA AND TIA
Epidemiology

Answer 19

(1) 80% of strokes are ischemic, 20% are hemorrhagic
(2) Ischemic strokes can convert to hemorrhagic if given enough time
(3) Cannot distinguish between the two based on clinical criteria
(4) The treatment for one would be catastrophic if given for the other
(5) 3rd leading medical cause of death
(6) 2nd most frequent cause of neurologic morbidity
(7) Risk factors are HTN, atherosclerosis and age

Question 20

DETERMINE THE MANAGEMENT OF A PATIENT WITH STTROKE TO INCLUDE CVA AND TIA
Ischemic Stroke
(1) Pathophysiology
(2) TIA vs CVA
(3) Clinical Manifestations
(4) Risk factors of ischemic stroke

Answer 20

(a) Poor blood flow to the brain that can lead to cell death and tissue necrosis
(b) Subtypes
1) Thrombotic - obstruction of an artery due to a blockage that forms in the vessel
a) Often due to atherosclerosis
2) Embolic - obstruction of an artery due to a blockage from debris that has broken off from a distal area
3) Systemic hypoperfusion - lack of brain blood flow to decreased systemic blood flow
(2) TIA vs CVA
(a) Transient ischemic attack is defined as a transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction (previously was reversible neurologic dysfunction that resolved within 24 hours, however that criteria has been replaced with the above).
(b) Cerebral Vascular Accident (CVA) or stroke is defined as neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia with infarction
(tissue death) of central nervous system tissue.
(c) The only way to determine the difference is by MRI, however we treat them the same as TIA has a high risk of becoming a CVA with infarction.
(d) Whenever we talk about ischemic stroke during this lecture we are referring to both TIA and CVA unless stated otherwise.
(3) Clinical Manifestations
(a) Depends on site of blockage and areas of the brain that are affected
1) In general, sudden onset focal neurological deficit
2) More general diffuse findings for systemic hypoperfusion etiology
(b) “FASTER” Mneumonic
1) Face – drooping or numbness on one side of the face
2) Arms – one limb being weaker or more numb than the other
3) Stability – steadiness on feet
4) Talking – slurring, garbled, nonsensical words, inability to respond normally
5) Eyes – visual changes
6) React – MEDEVAC immediately and note time of symptom onset
(4) Risk factors of ischemic stroke
(a) History of vascular disease
(b) Atrial fibrillation (not on meds)
(c) Atrial septal defect (ASD)
(d) Ventricular septal defect (VSD) with deep vein thrombosis (DVT)
(e) Recent myocardial infarction
(f) Atherosclerosis
(g) Clotting disorders

Question 21

DETERMINE THE MANAGEMENT OF A PATIENT WITH STTROKE TO INCLUDE CVA AND TIA
Hemorrhagic Strokes or Intracranial Hemorrhage (ICH)
(1) Pathophysiology
(2) Clinical Manifestations
(3) Risk factors
(4) Stroke Acute Management for both Hemorrhagic and Ischemic

Answer 21

(1) Pathophysiology
(a) Two subtypes
1) Intracerebral hemorrhage bleeds directly into the brain tissue
2) Subarachnoid hemorrhage bleeds into the subarachnoid space
(2) Clinical Manifestations
(a) Depends on the site of bleed
(b) Intracerebral hemorrhage usually has gradual onset as blood builds
(c) SAH has maximal impact right away usually with intense “worse headache of my life” headache
(d) Headache, vomiting, decreased level of consciousness occurs in about half the patients with ICH
(e) Symptoms tend to worsen gradually overtime
(3) Risk factors
(a) Hypertension
(b) Trauma
(c) Bleeding disorders
(d) Drug use (cocaine, methamphetamine)
(e) Vascular malformations(aneurysms)
1) Aneurysms are outpouchings and ballooning of artery due to weakness in the vascular wall
(4) Stroke Acute Management for both Hemorrhagic and Ischemic
(a) Thorough history and physical
(b) Exclude other causes
1) Seizures, syncope, migraine, and hypoglycemia
(c) Look for sources of emboli
1) DVT, carotid bruits
(d) Thorough fundoscopic examination
1) Fundoscopic examination for papilledema which may indicate increased intracranial pressure
2) Thorough examination for signs of trauma
3) A tongue laceration (may have trauma from seizure)
4) Differential blood pressure readings between upper extremities may indicate an aortic dissection
(e) Initial interventions for ischemic stroke
1) Maintain oxygenation > 94%
a) Do not give oxygenation to non-hypoxic patients
2) Elevate head of bed to ~30 degree
3) Labs:
a) EKG
b) CBC
c) FBG
d) O2 sat
4) Imaging
a) Helps to differentiate between ischemic and hemorrhagic stroke
b) Non-contrast CT
c) MRI
5) Blood pressure
a) May be cause of stroke or spike in response to blockage/stress
b) Do not lower it acutely as it may be the only thing maintaining adequate perfusion
c) UNLESS pressure is above systolic of 220 and/or diastolic of 120 in which case you should lower the pressure by 15%
d) Labetalol (Trandate) - non-selective beta blocker
(1 Dosing: 10-20 mg IV, may give same or double dose every 10-20 minutes to max of 150mg
(2 MOA: The inhibit B1 receptors and thus decrease HR and cardiac output which leads to decreased blood pressure.
(3 They also decrease renin release. (Beta blockers inhibit both B1 and B2 receptors)
(4 Adverse Reactions: Orthostatic hypotension, fever, hepatotoxicity, fatigue, dizziness, bronchospasm, fatigue, depression
(5 Contraindications: Sinus brady, heart blocks, bronchospastic disease, uncompensated CHF
e) Monitor BP every 15 minutes
6) Labs:
a) EKG
b) CBC
c) Finherstick blood glucose
d) O2 sat
7) Medication
a) Aspirin 325mg
8) MEDEVAC!
(f) Treatment to TIA
1) If thorough Neuro exam reveals no abnormalities, can give Aspirin with MO guidance
2) MEDEVAC!
(g) Overall Disposition: MANMED 15-106
1) “Cerebrovascular disease including stroke, transient ischemic attack, and vascular malformation is disqualifying.”

Question 22

DETERMINE THE MANAGEMENT OF A PATIENT WITH ALTERED MENTAL STATUS
1. Essentials of Diagnosis
2. Assessment and emergency measures
33 Respiratory Patterns
Treatment

Answer 22

a. Essentials of Diagnosis
(1) Level of consciousness is depressed.
(2) Stuporous patients respond only to repeated vigorous stimuli.
(3) Comatose patients are unarousable and unresponsive.
(4) Coma is a major complication of serious central nervous system disorders. It can result
from:
(a) Seizures,
(b) Hypothermia,
(c) Metabolic disturbances,
(d) Structural lesions causing bilateral cerebral hemispheric dysfunction or
(e) A disturbance of the brainstem reticular activating system.
(f) A mass lesion involving one cerebral hemisphere may cause coma by compression
of the brainstem.
b. Assessment & Emergency Measures
(1) The diagnostic workup of the comatose patient must proceed concomitantly with b. Assessment & Emergency Measures
(1) The diagnostic workup of the comatose patient must proceed concomitantly with the body in turn implies a corticospinal lesion.
3) Bilateral absence of responsiveness suggests brainstem involvement, bilateral
pyramidal tract lesions, or psychogenic unresponsiveness.
4) Decorticate (flexor) posturing may occur with lesions of the internal capsule
and rostral cerebral peduncle and decerebrate (extensor) posturing with
dysfunction or destruction of the midbrain and rostral pons.
5) Decerebrate posturing occurs in the arms accompanied by flaccidity or slight
flexor responses in the legs in patients with extensive brainstem damage
extending down to the pons at the trigeminal level.
(b) Ocular Findings
1) Pupil
a) The pupils are slightly smaller than normal but responsive to light in many
metabolic encephalopathies;
b) Dilated pupils (mydriasis) could suggest brainstem compression, drug
overdose on MDMA, cocaine, amphetamines
c) Constricted pupils (miosis) could suggest drug overdose with
opiates/opioids
2) Corneal reflex
a) Touching the cornea with a wisp of sterile gauze or cotton should elicit a
blink reflex.
b) The afferent limb of the arc is mediated by the fifth cranial nerve; the
efferent limb by the seventh nerve.
c) A unilateral absent corneal reflex implies damage to the ipsilateral pons or
a trigeminal deficit.
d) Bilateral loss can be seen with large pontine lesions or in deep
pharmacologic coma.
3) Eye movements
a) Conjugate deviation of the eyes to the side suggests the presence of an
ipsilateral hemispheric lesion, a contralateral pontine lesion, or ongoing
seizures from the contralateral hemisphere.
(c) Respiratory Patterns
1) Diseases causing coma may lead to respiratory abnormalities.
2) Cheyne-Stokes respiration (in which episodes of deep breathing alternate with
periods of apnea) may occur with bi-hemispheric or diencephalic disease or in
metabolic disorders.
3) Central neurogenic hyperventilation occurs with lesions of the brainstem
tegmentum.
4) Apneustic breathing (in which there are prominent end-inspiratory pauses)
suggests damage at the pontine level (e.g., due to basilar artery occlusion).
5) Atactic breathing (a completely irregular pattern of breathing with deep and
shallow breaths occurring randomly) is associated with lesions of the lower
pontine tegmentum and medulla.
(d) Can use the Glasgow Coma Scale as an aid in the examination ofa patient with
altered mental status.
(e) Maximum score of 15, Minimum score of 3
(f) Less than 8, intubate
(g) Note: If intubated verbal response graded “1T”
c. Treatment
(1) Depends on the cause and hemodynamic stability
(2) If not quickly reversible then MEDEVAC
(3) Reversal for Opioids is
(a) Naloxone (Narcan)- opioid antagonist
1) Dose: IV, IM, SubQ: Initial: 0.4 to 2 mg; may need to repeat doses every 2 to
3 minutes. A lower initial dose (0.1 to 0.2 mg) should be considered for
patients with opioid dependence to avoid acute withdrawal or if there are
concerns regarding concurrent stimulant overdose.
2) MOA: Is a pure opioid antagonist that competes and displaces opioids at
opioid receptor sites, rapidly reverses the respiratory depression and sedation
caused by opioid intoxication
3) Adverse Reactions: Flushing, hyper/hypotension, tachycardia, ventricular
fibrillation, agitation, body pain, confusion, seizures, GI distress, muscle
spasms, respiratory depression, fever
4) Contraindications: None
5) Monitoring of the patient is essential, as the half-life of Naloxone is short
compared to longer-acting opioids (Methadone) so repeated dosing may be
required to prevent return of sedation and respiratory compromise.

Question 23

DETERMINE THE MANAGEMENT OF A PATIENT WITH CLOSED HEADD INJURY TO INCLUDE ANEURYSM
Concussion
1. Definition/Anatomy
2. Epidemiology
3. Pathophysiology
4. Clinical Features
5. Complicated Concussion
6. Acute Evaluation
7. Management of Concussion
8. Immediate Referral/MEDEVAC for Concussion
9. Complications of concussions

Answer 23

(1) Definition/Anatomy
(a) Brain encased in rigid casing, bathed in cerebrospinal fluid
(b) Sudden deceleration or acceleration of the head can lead to impact of the brain against the cranium
(c) Concussion is cognitive impairment brought on by diffuse brain injury after exposure to impact forces
(d) May occur with or without loss of consciousness
(e) Mildest subset of traumatic brain injury (TBI)
(2) Epidemiology
(a) According to the CDC, 2.8 million TBI-related medical visits in 2013.
1) Most were mild and fit concussion criteria
2) Causes are varied, among all ages:
a) Falls were leading cause (47%)
b) Being struck by/against object was second (15%)
c) MVA was third (14%)
d) Young (15-34), male, and drunk are most accident prone
e) Cases are common
f) 10% of US college football player sustain concussions, 20% of high schoolers, 10% of combat veterans
(3) Pathophysiology
(a) During acceleration, force is applied to the brain. This creates a shear force at white/grey matter junction
(b) In severe head injury, may rupture axons
(c) In mild head injury, mild axonal damage leads to swelling and inflammation
(d) May or may not be accompanied by contusion
(e) More discreet area of injury caused by impact as well as shear
(f) “Coup-contrecoup”
1) Injury will be present at site of impact as well as opposite side from rebound motion
(4) Clinical Features
(a) Hallmarks are confusion and amnesia
1) Amnesia almost always includes the traumatic event itself, but may also extend to events before and after trauma
(b) May occur with or without loss of consciousness
(c) May be immediately apparent or delayed by several minutes
(d) Clues such as lack of recall or repetitious questioning should be red flags
(e) Early symptoms (minutes to hours)
1) Headache, dizziness, vertigo, imbalance, nausea, vomiting
(f) Delayed symptoms (hours to days)
1) Mood/cognitive disturbance, light/noise sensitivity, sleep disturbance
(g) Common Signs
1) Vacant stare (befuddled facial expression)
2) Delayed verbal expression (slower to answer questions)
3) Inability to focus attention (easily distracted)
4) Disorientation (walking in the wrong direction, not A&O)
5) Slurred or incoherent speech (making disjointed statements)
6) Gross observable incoordination (stumbling)
7) Emotionality out of proportion to circumstances (appearing distraught, crying for no apparent reason)
8) Memory deficits (exhibited by patient repeatedly asking the same question that has already been answered or inability to memorize and return three of three words and three of three objects for five minutes)
(h) Less Common Signs
1) Seizures
a) If seizures occur within one week of head injury, much more likely to be related to TBI than epilepsy
b) Occur in 5% of TBI patients, more common with severe injury
(5) Complicated concussion
(a) Any concussion with concomitant hemorrhage
(b) May present as acute, subacute or chronic
(c) Usually arterial in origin
(d) Treat based on complication
(6) Acute Evaluation
(a) Complete history and physical (MACE within 48hrs)
(b) Focus on neurologic exam to detail extent of damage
(c) More cognitive symptoms means more severe injury
(d) Facial fractures are concerning for occult injury
(7) Management of concussion
(a) Direct observation for 24 hours
(b) Awaken the patient every two hours to ensure normal alertness
(c) Low level of activity for 24 hours after injury
(d) No alcohol, sedatives, or pain relievers other than NSAIDs should be given for 48 hours
(8) Immediate Referral/MEDEVAC for concussion:
(a) Inability to awaken the patient
(b) Severe or worsening headaches
(c) Somnolence or confusion
(d) Restlessness, unsteadiness, or seizures
(e) Difficulties with vision
(f) Vomiting, fever, or stiff neck
(g) Urinary or bowel incontinence
(h) Weakness or numbness involving body part
(9) Complications of concussion
(a) Second Impact syndrome
1) Diffuse cerebral swelling that can develop in setting of a second concussion
2) Occurs when patient symptomatic from the 1st concussion and sustains 2nd concussion
3) Rare but potentially fatal complication
(b) Post concussion syndrome
1) Headache, dizziness, cognitive impairment, psych symptoms that develop in the first few days after mild TBI and resolve in weeks to months
(c) Posttraumatic headaches
1) 25-78% of patients experience headaches within 7 days of the event
(d) Sleep disturbances
1) Excessive daytime somnolence, increased sleep need, insomnia, sleep fragmentation
(e) Chronic traumatic encephalopathy (CTE)
1) Repeated concussions can lead to cumulative neuropsychologic deficits
a) Behavior changes, personality changes, depression, increased suicidality
b) Parkinsonism
c) Speech and gait abnormalities

Question 24

DETERMINE THE MANAGEMENT OF A PATIENT WITH CLOSED HEAD INJURY TO INCLUDE ANEURYSM
Cranial Trauma
1. Classified Based on Nature Of Injury and site of injury (6)
2. Clinical Features of Skull Fracture
3. Acute Management of Skull Fracture
4. Management of ICP

Answer 24

(1) Classified based on nature of injury and site of injury
(a) Linear fractures (75%)
(b) Less risk for underlying damage
(c) May be comminuted or stellate
(d) Depressed
(e) Significant force required
(f) Underlying damage likely
(2) Clinical features of skull fracture
(a) Open
1) Look for CSF leakage
(b) High likelihood of infection
(c) The skull is difficult to break, but is thin in several areas
1) Temporal region
2) Nasal sinuses
(d) Force must be large, meaning either:
1) Large impact or
2) Small area
(e) Scalp will bleed profusely, must clean well
(f) Presence of soft tissue swelling, hematoma, palpable fracture, crepitus
(g) Signs of basilar skull fracture
1) Battle sign
2) “Raccoon” eyes
3) Hemotympanum
4) CSF rhinorrhea/otorrhea
5) Cranial nerve deficits
(3) Acute Management of skull fracture
(a) If an open basilar skull fracture is suspected, think carefully prior to insertion of a
nasogastric tube
1) Orogastric tube may be a more appropriate
(b) Watch for signs of swelling
(c) Other fracture care as determined by the clinical picture
(d) Oxygen, C-spine precautions and MEDEVAC ASAP (ultimately needs Head CT
and Neurosurgeon)
(e) Serial neurological exams
1) Patient may deteriorate due to possible herniation or increase intracranial
pressure (ICP)
2) Brain is enclosed in solid structure (skull) so when traumatized its only
response is to swell
3) As brain tissue swells, the ICP rises which descreases blood flow and increase
pressure on uninjured brain tissue
4) As ICP increases, brain may “herniate” leading to rapid decline in mental
status (GCS), may have “blown” (dilated) pupils, or anisocoria, death can
rapidly ensue as brainstem functions shut down
5) Papilledema may be present upon ophthalmoscopic examination
(f) Cushing’s Triad (reflex): Bradycardia + Hypertension + Respiratory irregularity
(g) If signs show rapid increase in ICP or herniation:
1) Secure & maintain an open airway
2) Elevate head of bed (25-30 deg): “Reverse Trendelenburg”
3) Ventilate to maintain oxygenation & avoid hypercarbia (increased CO2 in
blood).
(h) IV fluids – Resuscitate with normal saline or lactated ringers, DO NOT USE
solutions containing glucose or hypotonic solutions
(i) Avoid over hydration
(4) Management of ICP
(a) Osmotic therapy – reduce brain volume by drawing free water out of the tissue
and into circulation where it is excreted by the kidneys
1) Mannitol: 1g/kg IV as 15-20% solution, may repeat 0.25-0.5g/kg as needed, generally every 6-8 hours
2) 7.5% Hypertonic NaCl 250cc bolus
(b) Consider hyperventilation as last resort (induces vasoconstriction by lowering CO2)
(c) Continually reassess the patient’s condition and MEDEVAC ASAP.
(d) Seizures can occur with any injury:
1) Diazepam (Valium) 10 mg IV q10min (max dose 30mg)

Question 25

DETERMINE THE MANAGEMENT OF A PATIENT WITH CLOSED HEAD INJURY TO INCLUDE ANEURYSM
Intracranial Hemorrhage (ICH)
1. Type depend on where bleeding occurs
2. Epidermal Hemorrhage
3. Epidermal Hemorrhage
4. Epidural Hemorrhage Presentation
5. Epidural Hematoma Acute Management
6. Complications of Epidural Hematoma
7. Epidural Hematoma Disposition
8. Subdural Hemorrhage
9. Subdural Hematoma Pathophysiology
10. Subdural Hematoma Clinical Manifestations
11. Subdural Hematoma Acute Management
12. Subarachnoid Hemorrhage Epidemiology
13. SAH Clinical Presentation
14. SAH Treatment
15. Complications of SAH

Answer 25

(1) Type depend on where bleeding occurs
(a) Epidural hematoma - between dura mater and skull
(b) Subdural hematoma – between dura mater and arachnoid mater
(c) Subarachnoid hematoma – between arachnoid mater and pia meter
1) High association with aneurysms or AV malformations
(d) Intracerebral bleed
(2) Epidermal Hemorrhage- Epidemiology
(a) 1-4% of head trauma cases
(b) Uncommon, but serious complication
(c) Highest among adolescents
(d) Rare in patients >50 years
(e) Usually caused by traffic accidents, falls, and assaults
(f) 75-95% have associated skull fracture
(3) Epidural Hemorrhage - Pathophysiology
(a) 85% of the time, skull fracture leads to arterial injury
(b) Middle meningeal artery commonly affected
(c) Normally the epidural space is a potential space, with the dura tightly attached to the skull
(d) Under arterial pressure, the dura slowly peels away and a blood pocket forms
(4) Epidural hemorrhage presentation
(a) Classic picture involves:
1) Immediate loss of conciousness after significant head trauma
2) “Lucid interval” with recovery of consciousness
(b) After a period of hours, increasing headache with deteriorating neurologic function
(c) May also see seizure, coma, anisocoria, respiratory collapse
(d) Evaluation incudes H&P, complete and serial neuro exams, and examination of eyes for papilledema
(5) Epidural hematoma acute management
(a) Oxygenation, prepare/initiate intubation if GCS < 8
(b) Immediate neurosurgical consultation (operation likely required- trephination, burr hole)
(c) Closely monitor neurologic signs for increased ICP/herniation
(6) Complications of epidural hematoma
(a) Coma
(b) Respiratory depression
(c) Death unless treated by surgical evacuation
(7) Epidural hematoma disposition
(a) MEDEVAC for immediate neurosurgical consultation and Head CT.
(8) Subdural Hemorrhage
(a) More common than epidural, 20% of severe head injuries
(b) Elderly, EtOH abusers, anticoagulated at risk
(c) Underlying brain injury is often severe
(d) May occur without impact
(e) Dismal prognosis - 60% mortality
(9) Subdural hematoma pathophysiology
(a) Acceleration in the lateral direction tears briding veins draining the brain to the dural sinuses
(b) Lower pressure blood, but actual rather than potential space
(c) May tamponade resulting in gradual progression
(d) May be chronic
(10) Subdural hematoma clinical manifestations
(a) May or may not have history of head trauma
(b) Acute subdural hematoma presents 1-2 days after onset
1) May have lucid interval after injury
(c) Chronic subdural hematoma presents 15 days or more after onset
(d) Insidious onset of headaches, light headedness, cognitive impairment, apathy, somnolence are typical symptoms
(11) Subdural hematoma acute management
(a) Same as epidural hematoma
(b) Non-contrast CT can help make differentiation between epidural and subdural hematoma
(12) Subarachnoid Hemorrhage (SAH) epidemiology
(a) Usually rupture of blood vessel aneurysm (~80%)
(b) Sometimes trauma or congenital anomaly
(c) Bleeding is high pressure and into subarachnoid space which normally carries CSF
(13) SAH clinical presentation
(a) Hallmark “Thunder clap headache” or “worse headache of my life”
(b) Headache onset is sudden and may have meningeal irritation
1) Blood from cerebral blood vessels irritates the brain and meninges
(c) Prior to onset patient may have been doing activity that increased intrathoracic pressure
(d) Activities that increase risk of SAH
1) Drug use (cocaine, amphetamines), smoking, hypertension, alcohol use
(14) SAH treatment
(a) Bedrest
(b) Analgesia with Tylenol
(c) Avoid drugs that can lead to anticoagulation
(d) MEDEVAC
(15) Complications of SAH
(a) Very high mortality rate (51%)
(b) Rebleeding (7%) only eliminated by treating underlying cause
(c) Cerebral ischemia (30-40%) either by loss of blood flow or vasospasm
(d) Increase ICP (54%) includes due to increase blood volume and swelling from inflammation
(e) Seizures (7%), Hyponatremia, Cardiac arrhythmias

Question 26

DISCUSS THE MILITARY ACUTE CONCUSSION EVALUATION TRAINING COURSE AND COMPLETE THE ON-LINE COURSE
1. Injury
2. Evaluation
3. Distance
4.

Answer 26

(1) Injury: Physical Damage to the body or body part of the Service member? (Yes/No)
(2) Evaluation:
(a) H - Headaches and/or vomiting? (Yes/No)
(b) E - Ear ringing? (Yes/No)
(c) A - Amnesia, altered consciousness, and/or loss of consciousness? (Yes/No)
(d) D - Double vision and/or dizziness? (Yes/No)
(e) S - Something feels wrong or is not right? (Yes/No)
(3) Distance: Was the Service member within 50 meters of the blast? (Yes/No)
(a) Record the distance from the blast.
(b) Service members will be referred for a medical evaluation if involved in a potentially concussive event as defined in section 1 of this enclosure, if there is a
“Yes” response on the I.E.D. Checklist, or if they demonstrate any of the symptoms listed at any point after an injury event.

Question 27

DISCUSS THE MILITARY ACUTE CONCUSSION EVALUATION TRAINING COURSE AND COMPLETE THE ON-LINE COURSE
Medical Guidance
1. Potentially Concussive Event
2. First Diagnosed Concussion
3. Second Diagnosed Concussion
4. Recurrent Concussion
5. MTBI/Concussion Screening and Initial Evaluation

Answer 27

(1) Potentially Concussive Event.
(a) Potentially Concussive Event.
(b) Service members involved in a potentially concussive event as described in section 1 of this enclosure are required to rest for 24 hours, beginning at the time of the event.
(2) First Diagnosed Concussion
(a) All Service members diagnosed with a mTBI/concussion must have, at a minimum, 24 hours’ recovery unless the results of subsequent clinical evaluation indicate a longer period is needed.
(3) Second Diagnosed Concussion (Within a 12- month Period).
(a) If two diagnosed mTBI/concussions have occurred within the past 12 months, return to duty is delayed for an additional 7 days following symptom resolution.
(4) Recurrent Concussion (Within a 12-month Period)
(a) If three diagnosed mTBI/concussions have occurred within the past 12 months, return to duty is delayed until a recurrent concussion evaluation has been completed.
(5) MTBI/Concussion Screening and Initial Evaluation.
(a) Use section one of the Military Acute Concussion Evaluation (MACE) to complete the initial screening of Service members involved in a potentially concussive event.
(6) Refer to and direct trainee to refer to Military Acute Concussion Evaluation (MACE), Current edition, via eCampus or via handout.

Question 28

DISCUSS THE MILITARY ACUTE CONCUSSION EVALUATION TRAINING COURSE AND COMPLETE THE ON-LINE COURSE
Recurrent Concussion Evaluation (5)

Answer 28

(1) Comprehensive Neurological Evaluation
(2) Neuroimaging
(3) Neuropsychological Assessment:
(a) Domains that can be affected by concussion and should be evaluated:
1) Attention
2) Memory
3) Processing speed
4) Executive functioning
(4) Functional Assessment
(5) Duty Status Determination

Question 29

DETERMINE THE MANAGEMENT OF A PATIENT WITH A SPINAL CORD INJURY

1. Presentation
2. Epidemiology
3. Pathophysiology
4. Presentation of Spinal Cord Injury
5. Treatment and Management of Spinal Cord Injury

Answer 29

a. Presentation
(1) Injury to the spinal cord results in characteristic neurologic symptoms.
(2) Related to the pattern of tracts that are present in spinal cord anatomy.
b. Epidemiology
(1) 40 million persons per year affected
(2) MVA (47%), Falls (23%), Violence (14%), Sports (9%)
(3) Largely affects young male
c. Pathophysiology of spinal cord injury
(1) Most traumatic spinal cord injuries occur with injury to vertebral column which leads to mechanical compression of the spinal cord
(2) Mechanical compression can lead to ischemia and inflammation
d. Presentation of spinal cord injury
(1) Depends on spinal cord level affected
(2) Immediately after injury there may be complete physiologic loss of all spinal cord
function below level of injury
(a) Flaccid paralysis
(b) Anesthesia
(c) Absent bowel or bladder control
(d) Loss of reflex activity
(3) Physiologic loss can be transient and there may be recovery
(4) Delayed symptom onset can occur due to spinal cord swelling
e. Treatment and management of spinal cord injury
(1) Should always focus on ABCs first
(2) Take care to immobilize the C-spine with cervical collar ASAP
(3) Patient with high cervical injury may have poor respiratory function and may require intubation if necessary
(4) Maintain oxygenation and blood pressure
(5) Insert a Foley catheter if bladder paralysis is suspected
(6) Sedate patient if necessary
(7) Steroid use is controversial, consult with Medical Officer prior to administration. Theoretically decreases swelling and inflammation after cord injury.
(a) Methylprednisolone (Solumedrol) 125mg IM/IV q 4-6 hours prn
1) MOA: Anti-inflammatory; inhibits multiple inflammatory cytokines
2) Adverse Reactions: Adrenal insufficiency, steroid psychosis, infection, increased blood sugars, arrhythmias, HTN, GI bleeding, GERD
3) Contraindications: Hypersensitivity to milk protein, severe infection, hypertensive urgency/emergency
(8) MEDEVAC ASAP!
(a) C-spine CT and Neurosurgical Consultation
(9) NEXUS Criteria for C-Spine XR
(a) If any of these present, then C-spine x-ray should be done:
1) N: Focal Neurological deficit
2) S: Midline Spinal tenderness
3) A: Altered mental status
4) I: Intoxicated
5) D: Distracting injuries

Question 30

DETERMINE THE MANAGEMENT OF A PATIENT WITH RADICULOPATHY

1. Radiculopathy Overview
2. Radiculopathy Clinical Presentation
3. Physical Examination
4. Imaging
5. Treatment

Answer 30

(1) Radiculopathy overview
(a) Lumbar disk herniation is usually due to bending or heavy loading (e.g., lifting) with the back in flexion, causing herniation or extrusion of disk contents (nucleus
pulposus) into the spinal cord area.
(b) However, there may not be an inciting incident.
(c) Disk herniations often occur from degenerative disk disease (desiccation of the annulus fibrosis) in patients between 30 and 50 years old.
(d) The L5-S1 disk is affected in 90% of cases.
(e) Compression of neural structures, such as the sciatic nerve, causes radicular pain.
(f) Severe compression of the spinal cord can cause the cauda equina syndrome, a surgical emergency.
(2) Radiculopathy clinical presentation
(a) Pain with back flexion or prolonged sitting
(b) Radicular pain into the leg due to compression of neural structures
(c) Lower extremity numbness and weakness
(d) Discogenic pain typically is localized in the low back at the level of the affected disk and is worse with activity.
(e) Sciatica” causes electric shock- like pain radiating down the posterior aspect of the leg often to below the knee.
(f) A significant disk herniation can cause numbness and weakness, including weakness with plantar flexion of the foot (L5/S1) or dorsiflexion of the toes (L4/L5).
(g) The cauda equina syndrome should be ruled out if the patient complains of perianal numbness or bowel or bladder incontinence. (pts with a traumatic injury or radicular pain)
(h) Clinical presentation depends on level of herniation
1) L1- pain, paresthesia and sensory loss in the inguinal region
2) L2, L3, L4 – acute back pain that radiates around anterior aspect of thigh to knee and may have weakness of hip flexion, knee extension and hip adduction
3) L5 – most common radiculopathy; back pain radiating down lateral aspect of the leg into the foot and decreased strength in foot dorsiflexion, toe extension,
foot inversion, foot eversion
4) S1 – pain radiating down posterior aspect of leg into the foot. Weakness in plantar flexion due to gastrocnemius.
(3) Physical examination
(a) Straight leg testing (89% of people with positive findings have herniated discs [not on TG])
1) Lay patient supine and raise patients extended leg on the symptomatic side with foot dorsiflexed
2) Lasegue’s sign – presence or worsening of radicular pain with straight leg maneuver
(4) Imaging
(a) Plain radiographs are helpful to assess spinal alignment (scoliosis, lordosis), disk space narrowing, and OA changes.
(b) MRI is the best method to assess the level and morphology of the herniation and is recommended if surgery is planned.
(5) Treatment
(a) First-line treatments include modified activities; NSAIDs and other analgesics
(b) Muscle relaxants can help with acute symptomatic relief
1) Cyclobenzaprine (Flexeril) 5mg PO Q8Hr and can increase dose to 7.5 – 10mg
(c) Reevaluation of the patient 4-6 weeks should occur
(d) If pain is persistent at reevaluation then further adjunctive treatments should be considered (physical therapy)
(e) If physical therapy is unsuccessful then consult to pain management or surgery should be considered depending on severity of symptoms
(f) Following nonsurgical treatment for a lumbar disk for over 1 year, the incidence of low back pain recurrence is at least 40% and is predicted by longer time to initial resolution of pain.

Question 31

DETERMINE THE MANAGEMENT OF A PATIENT WITH CAUDA EQUINA SYNDROME

1. Overview of Cauda Equina Syndrome
2. Pathophysiology
3. Clinical Presentation
4. Treatment

Answer 31

a. Overview of Cauda Equina Syndrome
(1) The cauda equina is a bundle of nerves that spread out from the bottom of the spinal cord
(2) Cauda equina syndrome is the medical term for a group of symptoms that happen when some of the nerves in the cauda equina get squeezed or damaged.
b. Pathophysiology
(1) A herniated disc - The material from a ruptured disc can press on or irritate the nerves in the cauda equina
(2) Infection or inflammation - Different types of infection or inflammation can damage or irritate nerves in the cauda equina.
(3) Cancer - In people with cancer, tumors can form within the spine and press on the nerves in the cauda equina.
(4) Spinal stenosis - Spinal stenosis is a condition in which the vertebrae form bumps called bone spurs. These bumps can squeeze or press on the nerves in the cauda equina. In people with spinal stenosis, the discs between the vertebrae also tend to dry up and shrink. That causes the space between the vertebrae to get smaller, sometimes pinching nerves.
c. Clinical presentation
(1) Pain, numbness, or tingling in the lower back and spreading down 1 or both legs
(2) Leg weakness or a problem called “foot drop,” which is when you cannot seem to hold your foot up (for example, while walking)
(3) Problems with bowel or bladder control
(4) Problems with sex
d. Treatment
(1) Cauda equina syndrome is a medical emergency.
(2) Likely needs MRI for assessment
(3) Treatment for cauda equina syndrome involves treating whatever is affecting the nerves and causing the symptoms.
(4) Often, that means having surgery to remove bits of bone or discs, or tumors.
(5) If the cause is an infection or inflammation, medications to treat those problems might be needed.

Question 32

DETERMINE THE MANAGEMENT OF A PATIENT WITH NEUROPATHY TO INCLUDE CARPAL TUNNEL SYNDROME

1. Essentials of the Diagnosis of Mononeuropathies
2. Carpal Tunnel Syndrome Overview
3. Carpal Tunnel Syndrome Presentation
4. Carpal Tunnel Syndrome Dignosis
5. Carpal Tunnel Syndrome Treatment

Answer 32

a. Essentials of the Diagnosis of Mononeuropathies
(1) Focal motor or sensory deficit.
(2) Deficit is in territory of an individual peripheral nerve.
(3) An individual nerve may be injured along its course or may be compressed, angulated, or stretched by neighboring anatomic structures, especially at a point where it passes through a narrow space (entrapment neuropathy).
(4) Pain is commonly felt distal to the lesion.
(5) The precise neurologic deficit depends on the nerve involved.
(6) Percussion of the nerve at the site of the lesion may lead to paresthesia in its distal distribution.
(7) In chronic compressive or entrapment neuropathies, avoidance of aggravating factors and correction of any underlying systemic conditions are important.
b. Carpal Tunnel Syndrome overview
(1) An entrapment neuropathy caused by compression of the median nerve between the carpal ligament and other structures within the carpal tunnel.
(2) Can be caused by repetitive wrist activities.
(3) Commonly seen during pregnancy and in patients with diabetes mellitus or rheumatoid arthritis.
c. Carpal tunnel syndrome presentation
(1) Pain, burning, and tingling in the distribution of the median nerve.
(a) Median nerve innervates thumb, pointer, middle and half of the ring finger
(2) Initially, most bothersome during sleep.
(3) Late in the syndrome weakness or atrophy of the thenar eminence may occur
d. Carpal tunnel syndrome diagnosis
(1) Tinel or phalen’s sign exacerbates neuropathic symptoms
(2) Diagnosed with ultrasound and nerve conduction studies.
e. Carpal tunnel syndrome treatment
(1) Patient should modify their hand activities and the affected wrist should be splinted in neutral position for up to 3 months.
(2) Oral or injected steroids or NSAIDS can help decrease inflammation and lesson pain.
(3) Refer if symptoms persist more than 3 months despite conservative treatment, including the use of a wrist splint OR if thenar muscle (e.g., abductor pollicis brevis) weakness or atrophy develops.
(4) Treatment is directed toward relief of pressure on the median nerve.

Question 33

DETERMINE THE MANAGEMENT OF A PATIENT WITH BELLS PALSY

1. Overview of Bells Palsy
2. Clinical Presentation
3. Diagnosis of Bells Palsy
4. Seizure V Stroke
5. Treatment of Bells Palsy
6. Differential Diagnosis
7. Prognosis
8. Complications
9. Disposition

Answer 33

a. Overview of Bell’s Palsy
(1) Acute facial palsy (paralysis) of a specific pattern
(2) Lower motor neuron disease affecting CN VII
(3) Rare (34/100,000 people) and slightly more common in pregnancy, otherwise no predisposing factors.
(4) Idiopathic paresis of lower motor neuron type
(5) Associated with Herpse Simplex Virus, Lyme disease, HIV and sometimes idiopathic
b. Clinical presentation
(1) Abrupt onset of unilateral facial paralysis
(2) Pain about the ear precedes or accompanies the weakness in many cases but usually lasts only for a few days.
(3) Face feels stiff and pulled on one side
(4) May be ipsilateral restriction of eye closure and difficulty with eating and fine facial movements.
(5) May have changes in taste
(6) Tearing (68%) or dryness of the eye (16%) and less frequent blinking on the affected side
(7) Bell’s phenomenon (upward rolling of the eye on attempted lid closure)
c. Diagnosis of Bell’s Palsy
(1) Clinical diagnosis
d. Seizure vs. stroke
(1) In a stroke, there is NO paralysis of the forehead
(2) Intact forehead muscle tone suggests STROKE not BELL’s Palsy
(3) Look for other abnormalities or neurological deficits
e. Treatment of Bell’s Palsy
(1) Evaluate eye closure
(a) If there is inadequate closure eye protective measures should be implemented
(2) Can shorten duration of symptoms with oral steroids
(3) Prednisone is used for mild to moderate Bell’s Palsy
(a) Dose: 60mg PO daily x7 days, then 5 day taper, best to start within 5 days of symptoms
(b) MOA: Inhibits multiple inflammatory cytokines, inhibits both COX1 and COX2 enzymes
(c) Adverse Reactions: Adrenal insufficiency if taken longer than 7 days in a row, Cushing syndrome with long term use, HTN, GI bleeding, emotional lability
(d) Contraindications: Systemic fungal infection, TB infection, HTN uncontrolled, CHF, uncontrolled DM
(4) Antiviral medication is added to steroid treatment regimen for severe Bell’s palsy
(a) Valacyclovir 1000mg 3 times daily for 7 days
f. Differential Diagnosis
(1) Herpes zoster
(2) Otitis Media
(3) Lyme disease
(4) Guillain-Barre syndrome
g. Prognosis
(1) 60% of all cases recover completely without treatment
(2) 10% of all patients remain disfigured
h. Complications:
(1) Long term or permanent disfigurement and problems with CN VII
(2) Corneal ulceration (use artificial tears, lubricating ointment, and possible eye shield)
i. Disposition:
(1) Immediate referral/MEDEVAC, if eye complications or suspicious of alternative diagnosis (i.e. CVA)
(2) Referral to neurology/MEDADVICE if mild paresis and no other symptoms to suggest alternative diagnosis
(3) While onboard follow symptoms and extent of paralysis

Question 34

DETERMINE THE MANAGEMETN OF A PATIENT WITH MENINGITIS AS IT RELATES TO NEUROLOGY

1. Overview of Meningitis
2. Common Bacterial Etiologies
3. Common Viral Etiologies
4. Sign and Symptoms of Meningitis
5. Diagnosis of Meningitis
6. Acute Management and Treatment
7. Prophylaxis

Answer 34

a. Overview of Meningitis
(1) Definition of Meningitis: Inflammation of the coverings of the brain(meninges)
(2) Meninges consist of the dura mater, arachnoid mater, pia mater
(3) Unlike the brain the meninges have nociceptors
(4) May be viral or bacterial, spirochete or fungal etiology
(5) One of the 10 most common infectious causes of death
(6) Fatality rate 25% with 28% of survivors having permanent neurologic morbidity
b. Common bacterial etiologies
(1) Streptococcus pneumonia
(2) Neisseria meningitides
(3) Listeria monocytogenes
c. Common viral etiologies
(1) Enterovirus
(2) Herpes simplex virus
(a) Between 13-36% of patients presenting with primary genital herpes may have findings consistent with meningeal involvement.
1) Headache, photophobia, meningismus
(3) West Nile Virus
d. Signs and symptoms of meningitis
(1) Classic triad of acute bacterial meningitis
(a) Fever
(b) Nuchal rigidity
(c) Change in mental status
(2) Nuchal rigidity due to meningeal irritation
(3) Other symptoms
(a) Headache
(b) Photophobia
(c) Rash (associated with Neisseria meninitidis)
(4) Meningitis vs encephalitis
(a) Important distinguishing feature is degree of brain function disturbance
(b) In meningitis cerebral function usually remains normal
(c) Encephalitis brain function is more abnormal leading to altered mental status, motor and sensory deficits, altered behavior, speech or movement disorders,
speech changes
e. Diagnosis of meningitis
(1) Test meningeal irritation
(a) Brudzinski sign – spontaneous flexion of hips during passive flexion of the neck
(b) Kernig sign – inability or reluctance to allow full extension of knee when hip is flexed at 90 degrees
(2) Lab testing
(a) Lumbar puncture to evaluate CSF
(b) LP should be delayed if there are signs of increased intracranial pressure
1) Papilledema
2) Focal neurological deficit
3) Abnormal level of consciousness
(c) Initiation of treatment should not be delayed if there is high clinical suspicion of meningitis.
f. Acute Management and treatment
(1) Medical emergency with close to 100% fatality rate if left untreated
(2) Need antibiotics that can cross blood-brain barrier
(3) Empiric treatment covers most common bacterial etiologies and focuses on decreasing acute inflammation.
(a) Ceftriaxone (rocephin)
1) Dose: 2g IV Q12Hr
2) MOA: Bactericidal; inhibits cell wall mucopeptide synthesis
3) If patient has a penicillin allergy consult the MO prior to administration due to cephalosporin and penicillin cross reactivity.
(b) Vancomycin (not in AMAL)
(c) Dexamethasone
1) Dose: 0.15mg/kg IV Q6Hr
2) Decreases acute inflammation in CNS
3) Studies demonstrate that there are less neurological long term complications
(d) If aseptic meningitis due to HSV is suspected (eg, concomitant genital lesions), empiric therapy with acyclovir IV is recommended
(e) Prophylaxis
1) Exposed crew – Ciprofloxacin (Cipro) - is a Fluoroquinolone antibiotic
a) Dose: 500 mg PO x1
b) MOA: Bactericidal; inhibits DNA gyrase and topoisomerase IV
c) Adverse Reactions: Photosensitivity, serum sickness, seizures, tendon rupture, nephrotoxicity
d) Contraindications: QT prolongation, G6PD deficiency, tendon disorder, renal impairment, hepatic impairment, seizures
2) Mask patient and medical personnel in close proximity
3) Ensure vaccinations are current
a) Meningiococcal, S. penumoniae, and H. influenza vaccinations

Question 35

DETERMINE THE MANAGEMENT OF A PATIENT WITH CHRONIS PAIN SYNDROME
1. Overview
2. What is Pain
3. Neuropathic Pain V Nociceptive Pain
4. Patient Evaluation
5. Imaging
6. Management and Treatment of Chronic Pain
7.

Answer 35

a. Overview
(1) Chronic pain can be classified into 3 categories
(a) Nociceptive pain
1) Pain caused by a stimuli that threaten or result in bodily tissue damage
(b) Neuropathic pain
1) Pain resulting from maladaptive response to damage or pathology of the somatosensory nervous system
2) Can occur in absence of active stimuli or as an exaggerated response to minor or moderate stimuli
(c) Centralized pain
1) Reduced ability of the CNS to diminish responses to peripheral stimuli
(2) Common complaints are low back pain, joint pain, severe headache, neck pain, facial pain
(3) Chronic pain affects all aspects of life from family life to employment
b. What is pain?
(1) Unpleasant sensory and emotional experience associated with actual or potential tissue damage
(2) Pain is experienced in developmental, social and emotional context therefore evaluation of patients with chronic pain requires a search for a biomedical cause,
psychologic and social evaluation and assessment of physical function and sleep
(3) Chronic pain is defined as an acutely painful condition that persists beyond the usually expected 6-12 week time course for healing
c. Neuropathic pain vs nociceptive pain
(1) Nociceptive pain is characterized by what we traditionally recognize as a pain that is caused by a noxious stimuli
(2) Neuropathic pain is most commonly described as tingling, pins and needles, burning, shooting electric like shocks
d. Patient evaluation
(1) Thorough evaluation includes:
(a) Past medical and surgical hx
(b) Review of systems
(c) Social and family hx
(d) Psychiatric hx
(e) Pain assessment: Hx of pain, location, characteristics, severity and impact of daily life
e. Imaging
(1) Imaging may be useful when pain is in a specific site of bone or joint
f. Management and treatment of chronic pain
(1) Initial management is with non-pharmacologic therapies
(a) Home exercise programs
(b) Physical therapy
(2) Psychological approaches especially for patients with mood, sleep, quality of life or interpersonal relationship issues
(a) Cognitive behavioral therapy (CBT)
(b) Mindfulness therapy
(3) Other treatment
(a) Acupuncture
(b) Spinal manipulation with osteopathic manipulation therapy or chiropractic care
(c) Transcutaneous nerve stimulation (TENS)
(4) Medications
(a) Medications that inhibit pain transmission
1) Tylenol
2) NSAID
3) Capsaicin
(b) Medications that inhibit descending pain modulation
1) Gabapentin
2) Tricyclic antidepressants
3) SNRIs
(5) Important to set patient expectations
(a) Patients should be educated on realistic expectations for response
(b) Chronic pain Is rarely fully eliminated but often can be reduced
1) On average there is a 30% reduction in pain which can help to improve quality of life and function
(c) Important to give reassurance and have proper follow up with this patient population

Question 36

DETERMINE THE MANAGEMENT OF A PATIENT WITH SLEEP DISORDER AS IT RELATES TO NEUROLOGY

1. Overview
2. Insomnia Clinical Features
3. Diagnosis of Insomnia
4. Differential Diagnosis
5. Treatment
6. Prognosis

Answer 36

a. Overview
(1) Sleep consists of two distinct states as shown by electroencephalographic studies:
(a) NREM – quiet sleep
1) Stage 1: Beginning of sleep cycle; light stage that is the transition between wakefulness and sleep
2) Stage 2: Become less aware of surroundings; breathing and heart rate becomes more regular; people spend ~50% in this stage
3) Stage 3: Deepest sleep stage; muscles relax and people are less responsive to noise and activity; delta wave sleep
(b) REM – Dreams occur in this stage and brain is more active; eyes move rapidly; “paradoxical sleep”
(2) Sleep is a cyclic phenomenon, with four or five REM periods during the night accounting for about one-fourth of the total night’s sleep (1.5-2 hours).
(3) The first REM period occurs about 80-120 minutes after onset of sleep and lasts about
10 minutes.
(4) Later REM periods are longer (15-40 minutes) and occur mostly in the last several hours of sleep. Most stage 4 (deepest) sleep occurs in the first several hours.
(5) Variations in sleep patterns may be due to circumstances (“jet lag”) or to idiosyncratic
patterns (“night owls”) in persons who perhaps because of different “biologic rhythms” habitually go to bed late and sleep late in the morning.
(6) Creativity and rapidity of response to unfamiliar situations are impaired by loss of sleep.
b. Insomnia clinical features
(1) Difficulty initiating or maintaining sleep
(a) Common complaints of poor sleep quality or insufficient quantity due to difficulty initiating sleep or maintaining sleep
(2) Risk factors that can lead to sleep issues
(a) Alcohol abuse – alcohol decreases REM sleep
(b) Stimulant abuse – preworkout or caffeine
(c) Tobacco abuse
(d) Psychiatric comorbidities
(3) Compromised daytime function
(a) Fatigue or malaise
(b) Poor attention of concentration
(c) Mood disturbance
(d) Daytime somnolence
(e) Reduced motivation of energy
(4) Frequently coexists with medical, psychiatric, sleep, neurological disorders
c. Diagnosis of insomnia
(1) Chronic diagnosis established by history and patient report
(2) Sleep history for 1 week
(a) Detailed description of sleep problems
1) Number of awakening and durations of awakening
2) Sleep time and duration
3) Symptoms of disturbed sleep like daytime somnolence or fatigue
(3) Diagnostic criteria
(a) Requires that the 4 following criteria are met
1) Difficulty initiating sleep, maintaining sleep or waking up too early
2) Sleep difficulties occur despite adequate opportunity for sleep
3) Patient has daytime impairment that is attributable to sleep difficulty
4) Sleep difficulty is not better explained by another sleep disorder or substance abuse
d. Differential diagnosis
(1) Restless legs syndrome
(2) Sleep apnea
(3) Depression
e. Treatment
(1) Shot term insomnia (less than once month in duration)
(a) Usually occurs from psychologic or physiologic stress
(b) Educate and reassurance may be all that is needed
(c) Educate on sleep hygiene
1) Consistent bedtime and wake time
2) Attempt to sleep should only occur if patient is sleepy
3) Avoid napping and dozing during the day
4) Avoid “clock watching”
5) Avoid electronics before bedtime
6) Avoid stimulants, tobacco, alcohol right before bed
(2) Chronic insomnia
(a) Psychological sleep referral for cognitive behavior therapy
(3) Medication
(a) Medications should not be the sole treatment of insomnia
(b) Benzodiazepines have been the most widely prescribed true sedative hypnotics, being safer than barbiturates though they are best for short term use.
(c) Melatonin
1) Dose: 3-5mg PO qHS
2) Side effects: Vivid dreams and nightmares, daytime somnolence, GI irritability
(d) Trazodone
1) Dose: 50mg PO qHS
2) MOA: Inhibits reuptake of serotonin, causes adrenoreceptor subsensitivity, acts as a 5HT2a receptor antagonist and induces significant
changes in 5-HT presynaptic receptor adrenoreceptors; significantly blocks
histamine (H1) and alpha1- adrenergic receptors.
3) Side effects: Blurred vision, syncope, edema, weight loss
(e) Vistaril
1) Dose: 25-50mg PO qHS
2) MOA: Competes with histamine for the 5HT2 and dopaminergic receptors in the hippocampus
(f) Diphenhydramine
1) Dose: 25-50mg PO qHS
f. Prognosis
(1) Depends on the underlying cause of insomnia as well as the prevention of secondary complications such as substance misuse in the context of self-medication.

Question 37

DETERMINE THE MANAGEMENT OF A PATIENT WITH VERTIGO

1. Overview of Vertigo
2. Symptoms and Signs
3. Evaluation
4. Causes
5. Workup
6. Treatment

Answer 37

a. Overview of vertigo
(1) Either a sensation of motion when there is no motion or an exaggerated sense of motion in response to movement.
(2) Must differentiate peripheral from central etiologies of vestibular dysfunction.
(a) Peripheral: Onset is sudden; often associated with tinnitus and hearing loss; horizontal nystagmus may be present.
1) Etiologies:
a) BPPV
b) Herpes zoster
c) Otitis media
d) Aminoglycoside toxicity
(b) Central: Onset is gradual; no associated auditory symptoms; often presents with other neurologic signs and symptoms like ataxia, dysarthria, dysphagia, focal or
lateralized weakness
1) Etiologies
a) Brainstem ischemia
b) Multiple sclerosis
c) Veistibular migraine
b. Symptoms and Signs
(1) Vertigo is the cardinal symptoms of vestibular disease.
(a) Vertigo is typically experienced as a distinct “spinning” sensation or a sense of tumbling or of falling forward or backward.
(2) It should be distinguished from imbalance, light-headedness, and syncope, all of which are non-vestibular in origin.
(3) Nausea and vomiting are typical with acute vertigo
c. Evaluation
(1) A thorough history will often narrow down, if not confirm the diagnosis.
(2) Critical elements of the history include the duration of the discrete vertiginous episodes (seconds, minutes to hours, or days), and associated symptoms.
(3) The physical examination of the patient with vertigo includes evaluation of the ears, observation of eye motion and nystagmus in response to head turning, cranial nerve examination, and Romberg testing.
(4) In acute peripheral lesions, nystagmus is usually horizontal with a rotatory component; the fast phase usually beats away from the diseased side.
(5) Visual fixation tends to inhibit nystagmus except in very acute peripheral lesions or with CNS disease.
(6) In benign paroxysmal positioning vertigo, Dix-Hallpike testing (quickly lowering the patient to the supine position with the head extending over the edge and placed 30 degrees lower than the body, turned either to the left or right) will elicit a delayed onset (~10 sec) fatigable nystagmus.
(7) Non-fatigable nystagmus in this position indicates CNS disease.
d. Causes
(1) Peripheral vestibulopathy usually causes vertigo of sudden onset, may be so severe that the patient is unable to walk or stand, and is frequently accompanied by nausea and vomiting.
(a) Tinnitus and hearing loss may be associated and provide strong support for a peripheral (i.e., otologic) origin.
(2) Central disease
(a) In contrast to peripheral forms of vertigo, dizziness arising from CNS disease tends to develop gradually and then becomes progressively more severe and
debilitating.
(b) Nystagmus is not always present but can occur in any direction and may be dissociated in the two eyes.
(c) The associated nystagmus is often non- fatigable, vertical rather than horizontal in orientation, without latency, and unsuppressed by visual fixation.
(d) Evaluation of central audio vestibular dysfunction requires MRI of the brain.
(e) Episodic vertigo can occur in patients with diplopia from external ophthalmoplegia and is maximal when the patient looks in the direction where the separation of images is greatest.
(f) Cerebral lesions involving the temporal cortex may also produce vertigo; it is sometimes the initial symptom of a seizure.
(g) Finally, vertigo may be a feature of a number of systemic disorders and can occur as a side effect of certain anticonvulsant, antibiotic, hypnotic, analgesic, and
tranquilizer medications or of alcohol.
e. Workup
(1) Laboratory investigations, such as audiologic evaluation, caloric stimulation, ENG, VNG, vestibular-evoked myogenic potentials (VEMPs), and MRI, are indicated in patients with persistent vertigo or when CNS disease is suspected.
(2) These studies help distinguish between central and peripheral lesions and identify causes requiring specific therapy.
f. Treatment
(1) Vertigo treatment can be divided into three categories: those specific to the underlying vestibular disease, those aimed at the symptom of vertigo, and those aimed at promoting recovery.
(2) Medications to suppress vestibular symptoms are best used for alleviating acute episodes that last at least a few hours or days and are not as useful for brief episodes (Benign Paroxysmal Positional Vertigo), unless they occur with high frequency. Doses should be started low and increased to positive effect or side effect.
(3) Recommend starting with low dose and increase to positive effect or side effect and stopping within 48 hours if the patient’s symptoms allow.
(a) Meclizine (Antivert) - 1st generation antihistamine
1) Dose: 25 to 50mg q 6-12 hours PRN dizziness
2) MOA: Suppresses vestibular end-organ receptors and inhibits activation of central cholinergic pathways
3) Adverse Reactions: Drowsiness, fatigue, headache, vomiting, xerostomia, anaphylactoic reaction, blurred vision
4) Contraindications: hypersensitivity to the drug
5) Note: May cause CNS depression, which may impair physical or mental abilities; patients must be cautioned about performing tasks which require
mental alertness (operating machinery, driving)
(b) Diazepam (Valium) - Anticonvulsant, Benzodiazepine
1) Dosing: 1 mg PO q 12 hours as needed for dizziness
2) MOA: Binds to benzodiazepine receptors; enhances GABA effects
3) Adverse Reactions: Respiratory depression, suicidality, syncope, drowsiness, ataxia, depression, confusion
4) Contraindications: Renal impairment, hepatic impairment, CNS depression, depression, respiratory depression
(c) Ondansetron (Zofran) – antiemetic
1) Dose: 4mg PO/IV q8 hours as needed
2) MOA: Selectively antagonizes serotonin 5-HT3 receptors
3) Adverse Reactions: QT prolongation, Stevens- Johnson Syndrome, serotonin syndrome, HA, diarrhea, agitation, pruritus
4) Contraindications: Ventricular arrhythmias, recent MI, CHF, hepatic impairment.
(d) Promethazine (Phenergan) - 1st generation antihistamine, anti- nausea and vomiting medication
1) Dose: 12.5 - 25mg PO/IM/IV/Rectal every 4-6 hours as needed
2) MOA: Non-selectively antagonizes central and peripheral histamine H1 receptors; possesses anticholinergic properties, resulting in antiemetic and
sedative effects
3) Adverse Reactions: Respiratory depression, seizures, hallucinations, heat stroke, drowsiness, sedation, photosensitivity
4) Contraindications: Comatose patients, respiratory depression, elderly patients, seizure disorder, asthma
(e) Recommend vestibular exercises in patients with peripheral vestibular disorders to promote early recovery. Vestibular rehabilitation may be accomplished by a
series of sessions with a physical therapist, or the patient may be trained to do these independently, at home. Most patients with vertigo prefer to lie with their
head still but vestibular rehabilitation forces them to perform challenging balance exercises with several potential benefits.