Neurosurgery

Question 1

GCS score

Answer 1

Eyes: 4 spontaneous, 3 to verbal command, 2 to pain, 1 don’t open.

Verbal: 5 oriented, 4 confused, 3 wrong words, 2 incoherent mumbling, 1 nothing.

Motor: 6 command, 5 localizes to pain, 4 withdraws from pain, 3 decorticate, 2 decerebrate, 1 flaccid.
(take best response from UE, legs can have reflex withdrawal even if brain dead).

Question 2

CN tests to r/o brainstem injury

Answer 2

Pupils: CN II and III (tests midbrain function).
Corneal reflex: test CN V and VII.
Gag reflex: tests CNIX and X

Question 3

Signs of uncal (transtentorial) herniation.

Answer 3

Lesions to lateral supratentorial region cause uncus of temporal lobe to herniate through tentorial notch. Stretch CNIII resulting in compression of CST (cerebral peduncle/cortex) on ipsilateral size.

SS:
CN III palsy (ipsilateral non-reactive dilated pupil, ptosis).
CST: contralateral hemiparesis.
Decreased LOC (GCS <15).

Question 4

Signs of acutely elevated ICP

Answer 4

Cushing’s triad: bradycardia, HTN with wide PP, irregular breathing.

Question 5

Abnormal breathing patterns and associated brain areas.

Answer 5

Cheyne stokes: irregular respiration with periods of apnea. Apnea -> hypercarbia/acidosis -> worsening cerebral edema/increased ICP. May involve bilateral hemispheres, diencephalon, upper midbrain.

Central neurogenic hyperventilation: low midbrain/upper pons.

Ataxic: completely irregular rate and volume or no breathing. Lower medulla.

Question 6

Immediate mxns of brain compensation for increasing ICP

Answer 6

Initially compensate by decreasing blood or CSF.
Ventricles become smaller and CSF is pushed down the spine. Dural venous sinuses become compressed .
Eventually can no longer compensate –> symptoms.

Question 7

Acute mgmt of closed head injury with potential increased ICP.

Answer 7

Airway: intubate if GCS <8 with C spine precautions. Insert nasopharyngeal airway if potential for tongue obstruction of airway. Ensure smooth intubation to prevent increased ICP due to gag, cough, struggle.

Breathing: maintain PCO2 at 30-35 mmHg (increased CO2 results in vasodilation to try to increase O2 to area and subsequently increases ICP more). If acutely decreasing GCS, transiently hyperventilate to avoid herniation.

Circulation: HTN and reflex bradycardia. Do not aggressively lower BP as it may cause ischemia (CPP = MAP - ICP). Maintain CPP >70 mmHg by keeping MAP >90 mmHg and ICP <20 mmHg.

Order CT head non-contrast.
CTA: look for injury to blood vessels including carotids, vertebral arteries. With very elevated ICP, won’t see blood flow to brain.

Question 8

Describe normal CPP autoregulation and how this changes with head trauma.

Answer 8

Autoregulation of CPP maintains CBF regardless of the MAP. With injury, lose autoregulation such that changes to CBF occur with changes to MAP.

Question 9

Conservative mgmt for elevated ICP

Answer 9

Elevate head of bed to 30*, neck in neutral position: increases intracranial venous outflow. Use reverse Trendelenberg if thoracolumbar spinal injury.

Prevent hypoTN w/ pressors, fluid.
Ventilate to normocarbia: prevent vasodilation of blood vessels which would increase blood flow to brain. Hyperventilate for brief periods only to prevent hypoxia.
Oxygen to maintain PO2 >60 mmHg and prevent hypoxic injury.
Osmolar diuresis with mannitol: draw fluid from the brain into the blood then cause diuresis. Is rapid acting. Need to keep sBP > 90 tho.
Steroids have NO role in initial mgmt closed head injury. Decrease edema over subsequent days.

Question 10

Aggressive mgmt closed head injury

Answer 10

Sedation or paralysis.
Draining CSF via ventriculostomy.
Barbiturate induced coma- reduce CBF and metabolism.
Decompressive craniectomy or lobectomy (last resort).

Question 11

Primary vs secondary head injuries

Answer 11

1: due to trauma, present at the time of impact. Irreversible. E.g. basal skull #, cerebral contusion, diffuse axonal injury, hematoma.
2: complication of the 1* injury.

Question 12

Give examples of secondary head injuries

Answer 12

1) loss of autoregulation –> edema, hydrocephalus.
2) increased ICP -> herniation, ischemia/hypoxia.
3) Delayed intracranial hematomas.
4) Meningitis.
5) Seizures.
6) Biochemical imbalance in neurons/glia –> acidosis, increased glutamate, Ca, free radicals, K+.

Question 13

Ways to prevent secondary head injuries

Answer 13

Prevent hypotension (pressors, fluids), hypoxia (give O2), hypercarbia (hyperventilate).
Early intubation/ventilation and fluid resuscitation important to prevent secondary brain injury.

Question 14

Know SS, pathophys and CT results of: epidural, SAH, subdural (acute/chronic) hemorrhages).

Answer 14

Epidural hemorrhage: skull # leading to bleed from middle meningeal artery. Blood pools between bone and dura. Pt may be lucid before decreased LOC. Hyperdense lens appearance (convex from skull), does not cross sutures. Tx with craniotomy.

SAH: can develop anywhere in brain. Look for hyperdense blood in sulci/gyri, ventricles.

Acute subdural: due to ruptured subarachnoid bridging vessels (usually arterial bleeding). Blood between dura and brain. No lucid interval (hemiparesis, pupillary changes). Look for hyperdense crescent on CT that is panhemispheric (over whole surface of brain). Treat with craniotomy if >1cm thick.

Chronic subdural hematoma: slow developing subdural. Occurs in elderly pts with brain atrophy, propensity to fall. Small initial acute SDH becomes chronic liquid blood with formation of surrounding membranes –> made of granulation tissue with small blood vessels prone to bleeding. Look for HYPODENSE crescent on CT.
Pts often asymptomatic or may have HA, confusions, signs increased ICP. ‘Mimicker’ of depression, dementia, focal deficits, increased ICP. Tx with burr holes or craniotomy if recurrent.

Question 15

Describe the clinical signs of the various basal skull #’s

Answer 15

Anterior fossa (orbital roof): periorbital hematoma (racoon eyes bilaterally), CSF rhinorrhea (# into paransal sinus with dural tear).

Petrous temporal bone: hemotympany, CSF otorrhea, mastoid bruising (delayed), facial nerve weakness (immediate or delayed), sensorineural hearing loss.

Scalp laceration: probe for underlying #.
CSF leak: usually will stop on its own.

Question 16

Important Q’s on Hx for head injury/potential brain lesion.

Answer 16

LOC and its length, amnesia (retro/antero-grade), associated seizure (high likelihood mass lesion), age >60 (more likely to have mass lesion/die from injuries), bleeding disorder/anticoagulation, HA, persistent vomiting.

Symptoms associated with mass lesions/delayed neurological deterioration: high speed MVA, rollover or pt ejected, death in same MVA, pedestrian struck, intoxicated pt, fall >3 ft or 5 stairs.

Question 17

Poor prognostic factors to consider with head injuries.

Answer 17

Low GCS on admission.
Absence of brainstem reflexes (pupillary, corneal, gag, occulocephalic).
Age >60.
Systemic insults: hypoxia, hypercarbia, hypoTN, prolonged seizure.
Penetrating head injury.

Question 18

SS of SAH

Answer 18

Sudden onset thunderclap HA. N/v, photophobia, meningismus (neck stiffness), decreased LOC, focal neurological deficits, sudden death.

Question 19

Common causes of SAH

Answer 19

Trauma.
Ruptured cerebral aneurysm (75%): sac-like outpouching of vessel wall at arterial bifurcation, thin secondary blebs may form at wall and rupture. Have close relationship with penetrating arteries. Most commonly affect main branches of Circle of Willis (ACA>PCA>MCA>carotid bifurc).
Other vascular malformations: usually cause ICH.
Vasculitis.
Bleeding disorders.
Hemorrhagic infarctions.
Angiogram negative- venous hemorrhage, much more benign.

Question 20

Investigative steps for suspected SAH.

Answer 20

CT head 1st line. Hyperdense cisterns and fissures on CT.

If CT head negative, do lumbar puncture for cell count. If there is blood in the CSF, compare amount in first to last tube. If traumatic tap, # blood cells should decrease by last tube. Can look for xanthochromia.

CTA.

Question 21

Mgmt SAH

Answer 21

BP control: sBP <140 to reduce risk of further bleeding.
Fluids and lyte monitoring (watch for SIADH).
ICP control: may require intraventricular drain.

Aneurysm tx:

1) microsurgical aneurysm clipping: craniotomy. Anatomical cure (definitive, durable). RIsk of vessel occlusion, perforation).
2) Endovascular aneurysm coiling (IR procedure): higher incidence of incomplete aneurysm occlusion. Potential for aneurysm recurrence and rebleeding.

Question 22

Complications of SAH

Answer 22

Aneurysm rebleeding.

Hydrocephalus.

Cerebral vasospasm: narrowing of arterial caliber due to irritation from blood outside the artery. Related to amt of blood on CT scan. Onset day 4-7 (new neurological deficit), may cause cerebral ischemia, altered LOC, fluctuating neuro deficits. Manage with CCB to reduce spasm, statins, hydration, ‘Triple H therapy’ –> HTN (sBP >180), Hypervolemia, Hemodilution which together act to force blood through vessels. Get gradual resolution over 2-3 weeks.

Question 23

RF for brain tumors

Answer 23

Ionizing radiation, genetic syndromes

Question 24

Presentation + initial tx of brain tumors

Answer 24

Increased ICP –> mass effect, edema, obstructive hydrocephalus. SS = HA (worse in morning, lying down, n/v), drowsiness, visual obscuration, papilledema, CN VI palsy (horizontal diplopia).
Tx w/ steroids to decrease edema, anticonvulsants.

If no focal deficits, consider frontal lobe tumors.

Mgmt: mgmt of symptoms, surgical resection, EBRT, chemo.

Question 25

What are the intra-axial tumors?

Answer 25

Tumors within the axis of the brain (true brain tumors), i.e. present within the parenchyma.
Primary:
1) Astrocytomas: glioblastoma multiforme = most common 1* tumor in adults. Craniotomy not curative, will recur. Use RT + chemo.
2) Oligodendroglioma.
3) Ependymoma

Secondary: lung, breast, melanoma. Make up half of brain tumors. Surgical resection with whole brain RT.

Question 26

What is an extra-axial tumor, give examples of primary, secondary.

Answer 26

Tumors that are outside of the axis of the brain: within the skull but not in the parenchyma. Push on and displace brain.

Primary:

1) Meningioma (most common extra-axial tumor), mostly benign with resection alone being curative.
2) Schwannoma
3) Pituitary adenoma
4) Craniopharyngioma

Secondary: very uncommon, if it occurs, breast ca.

Question 27

Symptoms of neurogenic shock

Answer 27

Hypotension (sBP <80), bradycardia, cutaneous vasodilation, wide PP, flaccid paralysis.
O/E: warm, dry skin, low JVP, priapism.

Caused by: interruption of SNS below level of injury. Results in unopposed PNS, loss of SNS tone. Loss of muscle tone results in skeletal muscle paralysis below level of injury causing venous pooling.

Question 28

What is spinal shock?

Answer 28

Transient loss of all neurologic function below level of SCI. Flaccidity with loss of reflexes and loss of visceral and peripheral autonomic control. Usually resolves within 48 hrs, sacral reflexes last to return. (I think resolves as in transitions to UMN symptoms).

Question 29

SS of: brown-sequard, anterior cord, central cord and posterior cord incomplete SCIs

Answer 29

Brown-Sequard: hemisection of cord. Causes ipsilateral motor dysfunction, contralateral pain/temp deficits, ipsilateral vib/proprioception deficits.

Anterior cord: vibration/priorioception and light touch preserved but lose motor control and pain/temp sensation below level of SCI.

Central cord: lose pain and temp at level of injury only. Lose motor control below injury. maintain vib/proprioception.

Posterior cord: lose vib/proprioception only below level of injury.

Question 30

Precautions to avoid further injury in pt with SCI.

Answer 30

Injury: cervical > thoracic > thoracolumbar junction > lumbosacral.

Mgmt:
ABC.
Immobilization: C spine collar, spinal board, brace, fixed immobilization (halo).
If hypoTN, maintain BP >90 with pressors, hydration, atropine.
Spine palpation: point tenderness or deformity.
Motor level assessment: including DRE.
Sensory level assessment: pinprick, light touch, proprioception.
Reflexes.
Autonomic dysfunction: altered level of perspiration, bowel or bladder incontinence, priapism.

Question 31

Precautions to avoid further injury in pt with SCI.

Answer 31

Injury: cervical > thoracic > thoracolumbar junction > lumbosacral.

Mgmt:
ABC.
Immobilization: C spine collar, spinal board, brace, fixed immobilization (halo).
If hypoTN, maintain BP >90 with pressors, hydration, atropine.
Spine palpation: point tenderness or deformity.
Motor level assessment: including DRE.
Sensory level assessment: pinprick, light touch, proprioception.
Reflexes.
Autonomic dysfunction: altered level of perspiration, bowel or bladder incontinence, priapism.

Imaging: 3 ciew C spine XR (AP, lateral and odontoid to visualize C1-C7/T1 junction. Flexion/extension view to look for occult instability.

Question 32

What to look for on assessment of spine via CT/XR w/ suspected SCI

Answer 32

Alignment: anterior vertebral line, posterior vertebral line, spinolaminar line, posterior spinous line.

Bone: vertebral bodies, facets, spinous processes.
Cartilage
Disc: disc space, itnerspinous space.
Soft tissue.

Question 33

What is radiculopathy and what are the SS?

Answer 33

Radiculopathy: nerve root compression, esp of cervical/lumbar roots.

Hx: LMN lesion signs, unilateral. Paresthesias, shooting pain, weakness, antalgic gait or flopping foot. Back pain with resolution followed by acute leg pain (suggestive of disc herniation).

PEx: will be specific to nerve root being compressed. Dermatomal/myotomal distribution. Radicular type pain. Absent reflexes, decreased tone, flaccid paresis, fasciculations.

Question 34

What is myelopathy and what are the SS?

Answer 34

Myelopathy = SC compression.

Hx: UMN lesion signs, global distribution, bilateral.
Weakness (difficulty going from sitting to standing), difficulty with buttons, writing, dropping objects. spastic gait, sensory changes such as numbness, tingling, burning, may have electric sensation due to irritation of PCML w/ flexion. Bladder symptoms such as urgency, urge incontinence.

PEx: sensory level cut off. In lower extremities, weakness of flexors > extensors. In UE, weakness of extensors >flexors. Hyperreflexia with increaesd tone, spasticity, clonus. Pathologic reflexes (upgoing plantar, Hoffmans), increased anal tone.

Question 35

Red flags on back pain history

Answer 35

'BACK PAIN'
Bowel/bladder incontinence/retention. 
Anesthesia (saddle). 
Constitutional symptoms/fever.
Khronic disease (hx malignancy)
Paresthesias. 
Age >50 yrs, <20 yrs. 
IVDU. 
Neuromotor deficits/night pain.

Question 36

SS cauda equina and mgmt

Answer 36

Compression of lumbosacral nerve roots below the conus medullaris (below L2 level).

Etiology: herniated disc, spinal stenosis, vertebral #, tumor.

SS: Acute (develops <24 hrs), sensory changes bilaterally (low back pain radiating to legs, aggravated by valsalva, sitting, bilateral sensory loss or pain), saddle anesthesia, autonomic (urinary retention and fecal incontinence), LMN lesion (weakness, paraparesis in multiple root distribution), reduced DTRs, sexual dysfunction.

Investigations: urgent MRI (confirm S2-4 compression), PVR to determine if true retention present.

Tx: surgical decompression within 48 hrs to preserve bowel, bladder, sexual function and prevent progression to paraplegia.

Question 37

Distinguishing features between neurogenic and vascular claudication.

Answer 37

Neurologic: ischemia of lumbosacral nerve roots secondary to vascular compromise and increased demand from exertion. Associated with lumbar stenosis. Has dermatomal distribution with positional relief occurring over minutes.

Palliation with bending over/sitting (flexion), provoked by walking downhill (extension), pulses/ABI normal, motor weakness after walking, no skin changes.

Vascular claudication: sclerotomal distribution with relief occurring with rest over seconds.

Palliated by stopping walking, provoked by walking uphill (flexion), reduced pulses/ABI, pain with cycling, skin changes. No motor weakness.

Question 38

Define cervical spondylotic myelopathy

Answer 38

SC becomes compressed due to wear and tear changes of spine. Cervical disc degeneration may be caused by bone spurs, herniation –> compression of SC.

Question 39

SS of cervical spondylotic myelopathy

Answer 39

Tingling/numbness in arms/fingers/hands, weakness in muscles of arms, shoulders, hands (trouble grasping/holding), imbalance, leg stiffness, loss of fine motor skills, pain or stiffness in neck.

Hyperreflexia, trouble walking, loss of balance, atrophy of hands.

Question 40

Etiology of SC compression

Answer 40

Disc herniation, ligamentous changes, facet hypertrophy, tumors, infection, alignment changes, cysts.

Question 41

Degenerative changes to the SC

Answer 41

Disc herniation: sciatica (80% improve with medical mgmt inc rest, NSAIDs, analgesics).
Foraminal stenosis.

Spondylolisthesis: slip of a vertebra in the AP direction. Narrows spinal canal and nural foramina. Decompression with laminectmy or foraminectomy can make slip worse (needs stabilization).

Scoliosis: decompression with fusion.

Spinal stenosis: narrowed spinal canal (bulging discs, facet joint hypertrophy, ligamentum flavum hypertrophy or buckling), symptomatic mgmt or laminectomy.

Question 42

Common tumors that involve the spine and the mxn that they cause SC or cauda equina compression.

Answer 42

Mets = most common.
Nerve root sheath tumors: Schwannoma (on the root), neurofibroma (within the root).

Cord tumors: glioma, epnedymoma, covernomas.

Primary bone tumors.