STUDY QUESTIONS IN THE TG Flashcards by Vince Le Tran

Structures that protect the CNS:

Mylination
Meningies
vetebral column
neuroganglia

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What are the three layers of the meninges?

Dura -outer
Arachnoid
Pia - covers the spinal cord/ brain

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Where is the CSF made and where is it reabsorbed?

Epidimal cells
choroid plexis
absorbed in the arachnoid villi

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Where is the CSF ciruclating in the CNS?

ventricles-> subarachnoid space to the villi

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Where does the spinal cord start and where does it end?

T1-L2

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What are the grooves that separate the spinal cord in halves?

anteror median fissure
posterior median sulcus

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What is the difference between the dorsal root and the ventral root?

ventral roots (anterior roots) allow motor neurons to exit the spinal cord.

dorsal roots (posterior roots) allow sensory neurons to enter the spinal cord.

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What are the different plexi of the spinal nerves and what parts of the body do they control?

Cervical Plexus—Serves the Head, Neck and Shoulders. …
Phrenic nerve (C3, C4, C5) innervates the diaphragm to contract.

Brachial Plexus—Serves the Chest, Shoulders, Arms and Hands. …Radial nerve (C5-T1), Ulnar nerve (C8-T1), Axillary nerve (C5- C6)

Lumbar Plexus—Serves the Back, Abdomen, Groin, Thighs, Knees, and Calves. …Femoral nerve (L2-L4)

Sacral Plexus—Serves the Pelvis, Buttocks, Genitals, Thighs, Calves, and Feet. Sciatic nerve (L4-S3)

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Why are T2-T12 different compared to other vertebral sections and what do they control?

intercostal nerves

Supply muscles of abdomen and between the ribs, skin of chest and back

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State the functions of the pathways in the spinal cord:

a. Corticospinal tract:
b. Spinothalamic tract:

a: Precentral Gyrus -> lower moter neurons intervates muscle movement

b: Sensory neurons touch, pain, temp towards the brain

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Posterior column-medial lemniscus pathway:
Brain
a. How much oxygen does the brain require and how long does it take for hypoxic damage to occur?

20% O2
Brain neurons deprived of oxygen for 4+ minutes may lead to permanent damage

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Blood brain barrier:
b. What cells make up the BBB?
c. What is the function?

Blood brain barrier protects the brain cells from harmful substances and pathogens.

(a) Allows passage lipid-solubleble materials such as O2, CO2, alcohol, anesthesia
(b) Consists of tightly sealed blood capillaries and astrocytes.
(c) Can be broken down by trauma, certain toxins, and inflammation.

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State of components and functions of the:
a. Brainstem (3 parts):
b. Limbic system:
c. Cerebrum:
d. Cerebellum:

Medulla Oblongata VIII-XII
a) Cardiovascular center regulates
b) Medullary rhythmicity area regulates breathing

Pons V-VIII
1) “Bridge”
2) Contains ascending (sensory) and descending (motor) tracts
3) Connects left and right sides of the brain
4) Nuclei
a) Motor relay from the cerebrum to the cerebellum
b) Helps control breathing

Midbrain III and IV
Cerebral peduncles: Large tracts that contain axons of motor neurons from the cerebrum to the rest of the brainstem and spinal cord

Limbic system:
emotional brain
involuntary survival behavior
part of memory development

Cerebrum:
Largest superior part
Corpus Callosum
Longitudinal Fissure -left and right hemi
Central sulcus- antieror/ posterior
Layers:
Cortex -grey matter
White matter
Basal Ganglia cognitive processes
Folds -gyri
shallow grooves - sulci
Prescentral gyrus anterior:motor
Postcentral gyrus posterior: somatosensory
Wernike’s -interpret
Broca’s - speech

Cerebellum:
Little brain
Fx equalibrium and coordination balance

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What are the components of the diencephalon and state significance of each part (there are 3 structures)?

Thalmus
-sensory relay center
-contributes to motor fx
-consciousness

Hyopthalmus
-homeostasis
-pituitary/ hormone production
-ANS
-eating drinking
-reg body temp
-reg sleep pattern

Pineal Gland
-melitonin

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Where are the following sensory areas:
a. Visual area:
b. Auditory area:
c. Gustatory area:
d. Olfactory area:

Occipital Lobe
Temportal Lobe
Postcentral Gyrus
Medial aspect of the temporal Lobe

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Where is the primary motor area?

Precentral Gyrus
Muscle movement duplicate voluntary

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What are the cranial nerves’ name and what are the function and components (i.e. purely
sensory, purely motor, or mixed)

CN1 S Olfactory-smell
CN2 S Optic - vision
CN3 M Ocularmotor
CN4 M Trochlear
CN5 B Trigeminal -chew ans general sensory
CN6 M Abducen
CN7 B Facial -taste, facial muscle
CN8 S Vesticolcholear -equalib, hearing
CN9 B -Glossophar - taste, bp swallowing
CN10 B - Vagus - sensory abd throrasic motor
CN11 M - Spinal Ass - trap and head movement
CN12 M - Hypoglossal- motor tongue

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Name the three neurons in the Somatic Sensory Pathway.

Cell body #1 in dorsal root ganglion

Cell body #2 in the spinal cord or brain stem

Cell body #3 in the thalamus; axon extends to the cerebral cortex (somatosensory area in postcentral gyrus)

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What reflex occurs at spinal nerve level T8, T9, and T10?

abdomen and/or lower in the back

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What reflex occurs at spinal nerve level L5, S1, and S2?

Plantar

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What are the subdivisions of the autonomic nervous system?

Sympathetic (S) division + parasympathetic (P) division

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Name the two neurons in the sympathetic division pathway.

Sympathetic preganglionic neurons
T1-L2 thoracolumbar division
Results in widespread S effects occurring simultaneously
epinephrine and norepinephrine

Sympathetic postganglionic neurons
S “trunk ganglia
pass back into spinal nerves

“prevertebral ganglia”
Supply abdominal viscera: stomach, intestine, kidneys, liver, spleen

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What does SLUDD stand for?

1) Salivation
2) Lacrimation
3) Urination
4) Digestion
5) Defecation

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How do we test for meningeal irritation? (know names of the tests and how to do them)

Positive Brudzinski and/or Kernig signs may indicate meningeal irritation.

Nuchal rigidity

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How do we test for balance?

Romberg Gait

How do we test deep tendon reflexes and how is it graded?

REFLEX SPINAL NERVE LEVEL EVALUATED Superficial Upper abdominal T8, T9, and T10 Lower abdominal T10, T11, and T12 Cremasteric T12, L1, and L2 Plantar L5, S1, and S2 Deep Tendon Biceps C5 and C6 Brachioradial C5 and C6 Triceps C6, C7, and C8 Patellar L2, L3, and L4 Achilles S1 and S2 GRADE DEEP TENDON REFLEX RESPONSE 0 No response 1 + Sluggish or diminished 2 + Active or expected response 3 + More brisk than expected, slightly hyperactive 4 + Brisk, hyperactive, with intermittent or transient clonus

What parts of the spinal cord do the following test: 1. Ankle: 2. Patellar: 3. Cremasteric:

Cremasteric T12, L1, and L2 Patellar L2, L3, and L4 Achilles S1 and S2

What are the symptoms of a seizure?

a) Facial grimacing b) Gesturing c) Lip smacking d) Chewing e) Repeating words or phrases

What are etiologies and risk factors that can lead to new onset seizure?

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

What is status epilepticus?

(EMERGENCY) A single seizure lasting more than or equal to 5 minutes or 2 or more seizures between which there is incomplete recovery of consciousness

What is the difference between partial and generalized seizures?

Partial One-sided 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 expected in this phase c) Episodes usually last 1-2 minutes

Describe the following: Tonic-clonic: Absence: Myoclonic: Complex partial: Simple partial: Psychogenic non-epileptic:

Focal seizure with retained awareness 1) Formerly known as simple partial seizure Focal seizure with impaired awareness 1) Formerly known as complex partial seizure 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 expected in this phase c) Episodes usually last 1-2 minutes Absence seizure causes you to blank out or stare into space for a few seconds. They can also be called petit mal seizures. Psychogenic nonepileptic 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

Describe post-ictal phase?

-Somnolence, confusion or headache that may occur for several hours -Patient often have no recollection of event -Weakness of limbs may occur (“Todd paralysis”)

What is the initial management and treatment for seizures?

1) First Aid 2) Treatment for active seizure Diazepam 5 mg IV/IM Q5-10 minutes; do not exceed 30 mg Valperic acid MEDEVAC immediately

(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)

Bell’s palsy Presentation:

(2) Lower motor neuron disease affecting CN VII (3) slightly more common in pregnancy (4) Idiopathic paresis of lower motor neuron type (5) Associated with Herpse Simplex Virus, Lyme disease, HIV and sometimes idiopathic Diabetis

Bell’s palsy Predisposing risk factors:

Clinical diagnosis

Bell’s palsy Diagnosis:

Mild to moderate (a) Prednisone 60mg PO daily x7 days, then 5 day taper; best to start within 5 days of symptoms Severe (a) Valacyclovir 1000mg 3 times daily for 7 days Eye Drops Immediate referral/MEDEVAC, if eye complications or suspicious of alternative diagnosis as Paresis (i.e. CVA)

Bell’s palsy Management/treatment:

“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

CVA Presentation:

Difference between bell’s palsy and CVA: Diagnosis:

(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

Difference between bell’s palsy and CVA: Management/treatment:

Fundoscopic examination Differential blood pressure readings between upper extremities Maintain oxygenation > 94% Elevate head of bed to ~30 degree 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

Difference between bell’s palsy and CVA: What is the target BP in case of ischemic stroke:

UNLESS pressure is above systolic of 220 and/or diastolic of 120 in which case you should lower the pressure by 15% Do not lower it acutely as it may be the only thing maintaining adequate perfusion

True vertigo is likely described as a spinning sensation rather than nonspecific lightheadedness. Trouble swallowing

TIA Presentation:

MRI Non-contrast CT

TIA Diagnosis:

Maintain oxygenation > 94% Elevate head of bed to ~30 degree Labs: a) EKG b) CBC c) FBG d) O2 sat Meds Labetalol (Trandate) - non-selective beta blocker (1 Dosing: 10-20 mg IV, may give same or double dose every 10-20minutes to max of 150mg Monitor BP every 15 minutes a) Aspirin 325mg If thorough Neuro exam reveals no abnormalities MEDEVAC!

TIA Management/treatment:

The disruption in blood supply results in a lack of oxygen to the brain. This can cause sudden symptoms similar to a stroke, such as speech and visual disturbance and numbness or weakness in the face, arms and legs.

TIA Complications:

(a) Fever (b) Nuchal rigidity (c) Change in mental status (3) Other symptoms (a) Headache (b) Photophobia (c) Rash (associated with Neisseria meninitidis)

Meningitis Presentation: Classic triad:

(1) Streptococcus pneumonia (2) Neisseria meningitides (3) Listeria monocytogenes (1) Enterovirus (2) Herpes simplex virus (3) West Nile Virus

Meningitis Common bacterial pathogens: Viral

(a) Brudzinski sign (b) Kernig sign Lab testing Lumbar puncture to evaluate CSF LP should be delayed if there are signs of increased intracranial pressure.

Meningitis Diagnosis:

Medical emergency with close to 100% fatality rate if left untreated Ceftriaxone (rocephin) 1) Dose: 2g IV Q12Hr Vancomycin Dexamethasone 1) Dose: 0.15mg/kg IV Q6Hr HSV is suspected (eg, concomitant genital lesions), empiric therapy with acyclovir IV is recommended

Meningitis Management/treatment:

Prophylaxis 1) Exposed crew – Ciprofloxacin (Cipro) - is a Fluoroquinolone antibiotic a) Dose: 500 mg PO x1 Meningiococcal, S. penumoniae, and H. influenza vaccinations for crew Masks

Meningitis Post exposure prophylaxis:

altered mental status, motor and sensory deficits, altered behavior, speech or movement disorders, speech changes

Encephalitis Presentation:

younger patients with encephalitis and associated seizures, movement disorders, and psychosis.

Encephalitis Risk factors:

intravenous acyclovir (10 mg/ kg every 8 hours for 10 days or more Long-term oral prophylaxis with valacyclovir

Encephalitis Initial management/treatment:

(a) Flaccid paralysis (b) Anesthesia (c) Absent bowel or bladder control (d) Loss of reflex activity

Spinal cord injury Presentation:

(1) Should always focus on ABCs first (2) Take care to immobilize the C-spine (3) intabation possible (4) Maintain oxygenation and blood pressure (5) Insert a Foley catheter if bladder paralysis is suspected (6) Sedate patient if necessary (7) Methylprednisolone (Solumedrol) 125mg IM/IV q 4-6 hours prn with MO advice Gi bleed (8) MEDIVAC

Spinal cord injury Initial management:

CASE 1 L5-S1 disk is affected in 90% of cases. (a) Pain with back flexion or prolonged sitting (b) Radicular pain into the leg due to compression (c) Lower extremity numbness and weakness (d) Discogenic pain typically is localized (e) Sciatica” causes electric shock (a) Straight leg testing (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 Physical Therapy CASE 2 Clinical presentation (1) Pain, numbness, or tingling (2) Leg weakness or a problem called "foot drop," (3) Problems with bowel or bladder control (4) Problems with sex Treatment (1) Cauda equina syndrome is a medical emergency. (2) surgery

Spinal cord injury Complications: Radiculopathy Cauda Equina Syndrome

Hallmarks are confusion and amnesia 1) Amnesia almost always includes the traumatic event itself but may also extend to events before and after trauma (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 3) Inability to focus attention (easily distracted) 4) Disorientation 5) Slurred or incoherent speech 6) Gross observable incoordination 7) Emotionality out of proportion to circumstances 8) Memory deficits

Concussion/TBI Presentation:

Injury will be present at site of impact as well as the opposite side from the rebound motion

Concussion/TBI Explain coup-coutrecoup:

(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

Concussion/TBI Management/treatment:

Clues such as lack of recall or repetitious questioning should be

Concussion/TBI Red flag signs/symptoms:

24hr

Concussion/TBI How long must the patient rest after an injury?

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.

Tension headache Presentation:

(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

Tension headache Risk factors:

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 Tylenol (1 Dose: 325-1000 mg PO q 4-6 hours, max 4 grams/24 hours

Tension headache Management/treatment:

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

Cluster headache Presentation:

Contraindications: Ischemic heart disease or signs or symptoms of ischemic heart disease (

Cluster headache Risk factors:

CT MRI office visit

Cluster headache Diagnostic testing:

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; 4) Oral Zolmitriptan (Zomig) – Oral anti-migraine medication if they are able to tolerate. a) Dose: Initial: 2.5 mg

Cluster headache Management/treatment:

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 4) Family history often positive for headaches 5) May have associated nausea and vomiting

Migraine 1. Presentation (Quality and descriptors of HA

Migraine Risk factors:

During acute attacks - rest in a quiet, darkened room until symptoms subside. 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 Sumatriptan (Imitrex) (1 Dosing: Oral: A single dose of 25 mg, 50 mg, or 100 mg Zolmitriptan (Zomig) a) Dose: Initial: 2.5 mg, may repeat if needed 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) Antidepressants a) Amitryptyline Start at 10mg at bedtime; dose range 20-50mg at bedtime Anticonvulsants: a) Topiramate (1 Dose: 100-200mg a day 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

Migraine Treatment:

((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

Subarachnoid hemorrhage Presentation:

Activities that increase risk of what 1) Drug use (cocaine, amphetamines), smoking, hypertension, alcohol use

Subarachnoid hemorrhage Risk factors:

CT MRI

Subarachnoid hemorrhage Diagnostic testing:

(a) Bedrest (b) Analgesia with Tylenol (c) Avoid drugs that can lead to anticoagulation (d) MEDEVAC

Subarachnoid hemorrhage Management/treatment:

(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

Epidural hematoma Presentation:

Highest among adolescents 75-95% have associated skull fracture Usually caused by traffic accidents, falls, and assaults Uncommon, but serious complication

Epidural hematoma Predisposing risk factors:

between dura mater and skull

Epidural hematoma Source of bleed:

Non-contrast CT

Epidural hematoma Diagnostic testing:

(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

Subdural hematoma Presentation:

(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

Subdural hematoma Predisposing risk factors:

between dura mater and arachnoid matter

Subdural hematoma Source of bleed:

Non-contrast CT can help make a differentiation between hematoma

Subdural hematoma Diagnostic testing:

(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 SAME AS EPIDURAL

Subdural hematoma Management/treatment:

(a) Open (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

Basilar skull fracture Presentation:

1) Battle sign 2) “Raccoon” eyes 3) Hemotympanum [ear blood] 4) CSF rhinorrhea/otorrhea [liquid from ears or nose] 5) Cranial nerve deficits

Basilar skull fracture Physical exam findings indicating fracture:

Orogastric tube may be a more appropriate

Basilar skull fracture Management/treatment: