169. Central Nervous System Procedures and Devices

Lumbar Puncture

C/I: skin infection, increased ICP, platelets <20k, >50k are safe, INR > 1.5, heparin/lovenox <24hrs, hemophilia, vW dx, other coagulopathies, trauma to lumbar vertebrae.

Transverse line thru iliac crests is L4 spinous process. Go above (L3-L4) or below (L4-L5). Direct needle toward umbilicus. The ‘pop’ is usually the ligamentum flavum.

US used to identify interspace; not to guide the procedure (basically better able to see midline of spinous processes and where they are in obese patient).

Opening pressure (normal 50-170mmH20) must be measured with patient in lying in extended position; not curled position or it could be artifically elevated. Careful repositiong (straightening of curled patient vs helping the seated patient to a lying position on his side) can be safely performed with the needle in place.

Complications: Post-LP headache (continuous CSF leakage from dural puncture site) – begins 24-48 hrs after procedure – usually frontal or occipital; pressure-like. Worse with patient sitting/standing upright and with Valsalva/coughing. Improves with patient supine. IV caffeine (500mg IV of caffeine sodium benzoate) is common tx. Persistent headache can be treated with epidural blood patch.

CSF Shunts

Silastic tube passed into ventricle via burr hole – tunnels to valve chamber (establishes pressure gradient that allows drainage away from ventricle) – distal tubing goes to drainage point. MC site peritoneal cavity. Can also be right atrium, gallbladder, pleural cavity, ureter. Dials on valve are usually radiopaque can pressure settings can sometimes be seen. MRI can sometimes adjust the valve so settings need to be verified afterward.

Complications: Obstruction (MC proximal tubing), usually within first year. Distal obstruction more common after >2y since placement. Present with increased ICP: headache, lethargy, nausea/vomiting, CN palsies.Fracture (of tubing) – occurs usually over clavicle or distal ribs.

Slit Ventricle Syndrome: overdrainage where elevated ICP eventually leads to drainage again until it hits a point. Will be cyclical – waxing/waning.

Decreased LOC is usually MC sign for malfunction. As ICP increases, paralysis of upward gaze (sundowning), dilated pupils, papilledema.

For simple device, pressing on chamber and observing refill is normal. Difficulty compressing might mean distal flow obstruction whereas slow refill > 3s might indicate prox obstruction. 40$ of obstructed shunts though can have normal refill during manual palpation.

Shunt series: AP/lateral skull, AP chest/abdomen looking for kinking/migration.

CT: ventricular size – need to compare priors since baseline ventricular size is usually abnormal. 24% of documented shunt malformation showed no evidence of malfunction on CT. CT/xray can not be relied on to rule out malfunction in the appropriate clinical setting. Basically always call NSGY, particularly if you are really suspecting it.

Do tap shunt unless life threatening ICP situation. Measure pressure with LP manometer sterilly. Should be 12 +- 2.  Distal obstruction = high H20, proximal obstruction = low H20. Remove slowly to prevent choroid plexus bleeding.

Shunt Infection: 50% occur within first 2 weeks after revision/placement, 70% within 2 months. Usually in very young/old. Higher incidence of meningitis (similiar bugs: Strep pneumo, N.meningitidis). Usual shunt infections caused by staph epidermidis; also Staph aureus and propionibacterium acnes. GN have high risk mortality.

Nonspecific symptoms: headache, AMS, n/v, neck stiffness, fever. Rule out with shunt tap. LP misses shunt infections. Cultures still grow in 1/5 of patient despite normal initial CSF analysis. Treat early with typical meningitis coverage (Vancomycin + Rocephin).

Halo Devices

Rigid cervical immobilization. Used for stabilization of unstable cervical spine fractures/dislocations/subluxations. Not used when distal sensory deficit (unable to detect skin breakdown). 4 pins usually placed in thick portions of skull.

Complications: pin loosening – check for infection; if there is movement of cervical spine, need to apply alternative measure (aspen collar) while waiting on NSGY consult and xrays. Pin site infections occur 50% within first month. Typical pin site infections require typical wound care, treatment for staph/strep if warranted. Pain with mastication usually due to too lateral placement of pins into the temporalis muscle. Dysphagia due to extreme extension of neck. Can also occur with anterior displacement of bone graft.

Intrathecal Baclofen Infusion Devices

Baclofen: GAMA agonist that acts on level of spinal cord to decrease spasticity, improves gait, sitting ability and upper extremity function. Withdrawal symptoms: extreme hypertonicity and spasma which can lead to rhabdo. Treat with oral baclofen, oral or IV benzos.

Implantable CNS Stimulators

Help with Parkinsons resistant to medications. High frequency stimulation in the subthalamic and globus pallidus interna. Consider lead displacement or migration. Consider turning off the stimulator to sort of acute CNS abnormalities.

Spinal Cord Stimulation

Treatment for chronic back pain. Multiple contact points are placed in epidural space and hooked up to pulse generator. Complications include dura puncture, spinal cord compression, CSF leak. MC complication is device failure.


Tintinalli, Seventh Edition, Chapter 169: Central Nervous System Procedures and Devices

169. Central Nervous System Procedures and Devices

168. Central Nervous System and Spinal Infections

Meningitis: inflammation of the meninges.

Encephalitis: inflammation of part of the brain (any part).

Presentation: Fever, neck stiffness, and mental status changes. 50% have all three. When adding headache, patients with meningitis have 95% chance of presenting with >2 of the 5.

Start antibiotics as soon as you’re thinking of bacterial meningitis.

Start empiric steroids. If youre thinking bacterial meningitis, you need to start steroids. If you’re pretty confident on viral or HSV, you can hold off. Give dexamethasome while you’re figuring it out.

Don’t delay antimicrobials for the CT or LP. CSF becomes sterilize after 6 hours after IV abx.

Do you CT before every LP? If AMS, focal neuro deficits, papilledema, new onset seizures, hx/o neuro dx or immunosuppression.

Get opening pressure if you can.

Normal CSF:< 50 protein, < 5 WBCs, no RBC, no organisms.

Bacterial Meningitis: < 2/3 glucose, > 50 protein, > 100 WBC, few RBCs, organism seen on 70% cases.

Viral Mengingitis: normal glucose, normal protein, > 10 WBC (lymphs), few RBCs, no organisms on gram stain.

Herpes encephalitis: > 2/3 serum glucose, < 50 or > 50 protein, > 100 WBC, > 10 RBC, no organisms on gram stain. Seen in elderly with headache/fever.

Two criteria: Reller Criteria (elevated CSF cell count >5, elevated CSF protein >50, immunocompromised (HIV or transplant), age <2yo) and Bouza Criteria (elevated CSF WBC count >10, immunocompromised (HIV or transplant), and age <2yo). If meet criteria, likely start acyclovir before getting back CSF PCR. Acyclovir can be nephrotoxic and increase seizure threshold. (PulmCrit, 2017)

If meningococcus, remember exposure prophylaxis.


Meningitis and Encephalitis, Michael Abraham, The Crashing Patient Conference 2015.


168. Central Nervous System and Spinal Infections

167. Chronic Neurologic Disorders

Amyothrophic Lateral Sclerosis (ALS)

Rapidly progressive upper/lower motor neuron weakness. Thought to be genetic mutation.

Upper motor neuron demyelination: limb spasticity, hyperreflexia, emotional lability. Positive Babinski sign (fans out)

Lower motor neuro demyelination: limb muscle weakness, atrophy, fasiculations, dysarthria, mastication difficulty.

Cognition and sensory findings usually still intact. Progression over weeks/months to the point of respiratory failure.

Tx: supportive; prevent aspiration, look for signs of impending respiratory failure. Riluzole is a excitotixin glutamate modulation medication that can increase survival.

Myasthenia Gravis

Autoimmune disease; Acetylcholine receptor antibodies (AChR) form; proximal muscle weakness. Thymus abnormal in 75% of patients.

General weakness of proximal muscle groups including neck extensors, facial/bulbar muscles, ptosis (eyelid drooping), diplopia, dysphagia/dysarthria, dysphonia.

Diagnosis: Edrophonium chloride administration (improvement in symptoms after receiving medication though can cause worsening weakness if given to someone with other disorder of neuromuscular impairment). EMG does repetitive nerve stimulation. AChR antibody testing is blood test, though early MG will have 15% false negative.

Treatment: Thymus removal. Patients usually on pyridostigmine 60-90mg q4hrs and should get it scheduled. If miss a dose, double the next. If need to give IV, give 1/30th dose (2-3mg). Neostigmine is usually 0.5mg.

Avoid neuromuscular blockers (paralytics) since it will last 2-3x longer. Consider using 1/2 regular dose.

Myasthenic Crisis vs Cholinergic Crisis: give 1-2mg slow IV push of edrophonium (rapid onset of 30s, duration 5-10m). If showing improvement, continue giving up to 10mg, then give neostigmine 0.5-2mg IM/SC which will last for 4 hours. If worsening with edrophonium, likely cholinergic and consider giving atropine or intubating.

Multiple Sclerosis 

Inflammatory disorder; scattered neuron demyelination. Can affect multiple areas including cerebrum, brainstem, spinal cord, and cranial nerves.

Lower extremity symptoms more severe than upper extremity. Young person with multiple neuro systems of different areas over time. Lhermitte sign: electrical shock sensation/pain down back/arms/legs with flexion of the neck. Dysautonomias: urinary retention, urgency/frequency, stress incontinence. Paresthesais, gait disturbances, extremity weakness, poor coordination, visual disturbances.

Optic neuritis: 30% initial sign. Unilateral vision loss, retrobulbar pain, afferent pupillary defect (Marcus Gunn pupil).

Symptoms worse with body temp increases (fever, exercise, hot bath). Diagnosed by T2 weight MRI findings of multiple discrete lesions on white matter, including in spinal cord.

Treatment: glucocorticoids, interferon-B. High dose steroids for exacerbations. Exclude causes of stress/infection. Due to post void residual, very common to have UTI/pyelo.

Lambert-Eaton Myasthenic Syndrome

Autoimmune disorder like MG causing flucutating weakness/fatigue in proximal limb muscles. Show some improvement in strength with sustained/repeated exercises like MG. Lambert sign: squeeze strength increases over a few seconds.

Associated with malignancy (50% has small cell lung cancer). Predominant in older men with hx/o smoking.

Treatment supportive, though can be similar to MG (tx cancer, neostigmine, steroids).

Parkinson’s Disease

 Lewy bodies: cellular cytoplasmic inclusions; in the midbrain, particularly in the substantia nigra. Results in loss of fucntional dopaminergic receptors, resulting in lower dopamine levels.

TRAP: resting tremor (pill rolling, not with movement), cogwheel rigidity (intermittent stiffness with passive ROM of the extremities), bradykinesia or akinesia (slowness, inability to perfom), impairment of posture/equilibrium (hard time turning/changing directions, lose balance). Clinical diagnosis primarily.

Treatment: Reduce symptoms: anticholinergics (benztropine), central dopamine increasing medicatiosn (levodopa, carbidopa), dopamine receptor agonists (bromocriptine).

Levodopa SE: anorexia, nausea/vomiting. Carbidopa decrease these SE. Effects of medications will decrease overtime. On-off phenomenon can occur where patient pretty debilitated in the morning before receiving medications. Drug holiday (off medication for 1 week) can sometimes increase effect of medication when it is started again.

Dopaminergic therapy toxicities: cardiac dysrhytmias, orthostatic hypotension, dyskinesias, dystonia. Psychosis/hallucinations can be caused by dose and having reduction in medications can help reduce these symptoms.

Psychotropics (haldol) can have increased likelihood of tardive dyskinesia.

Poliomyelitis and Postpolio Syndrome

Poliomyelitis: enterovirus infection, causing striated muscle paralysis in <5% of patients. Usually just GI viral illness in most patients affected. After typical viral illness, asymeetric proximal limb weakness in lower extremities. Flaccid/weak muscles, absent tendon reflexes, fasiculations. Sensory deficits usually not present. Usually occurs over 5 days, then wasting occurs over several weeks.  CSF will show pleocytosis. Throat/rectal swaps for disease are more accurate in early course of disease.

Postpolio syndrome can occur 20-35 years after initial benign infection (though would usually be in patients > 50-60yo). Muscle fatigue, joint pain, worsening skeletal deformities. Patients usually had neuro symptoms with initial infection 30 years ago. Lamictal can sometimes help recovery in postpolio syndrome.

GBS usually presents very similar, though symmetric muscle weakness unlike polio which is unilateral.


Tintinalli, Chapter 167: Chronic Neurologic Disorders


167. Chronic Neurologic Disorders

166. Acute Peripheral Neurologic Lesions

Central vs Peripheral Weakness?

Brain/Spinal Cord: Upper Spinal Motor Neuro Lesion: Tone goes up, reflex goes up, babinski upgoing, no wasting, no fasiculations. Not really useful in the acute setting.

Motor weakness: look at distribution: clinical localization, proximal vs distal, facial involvement, symmetry, progression. Sensory, reflexes.

If reflexes present, it is NOT: GBS, NMJ blocker, botulism, hypermagnesium.

Guillain-Barre syndrome: acute inflammatory demyelinating polyradioculopathy. Weakness more proximal, Legs>arms, symmetrical. Rapid, ascending. 2-4 weeks after URI/GI illness.

Myasthenia Gravis: 85% eye involvement, gradual. precipitated by medication noncompliance, infection (usually pneumonia).

Spinal Cord: acute compression from epidural compression, epidural abscess, tumor. Acute ischemia/infarct from aortic dissection. Weakness below lesion of lesion, usually symmetric.

Anterior spinal artery syndrome: less of pain/temp sensation lost, others preserved.


Acute Non-traumatic Weakness, Danya Khoujah, The Crashing Patient Conference 2015.

166. Acute Peripheral Neurologic Lesions

165. Seizures and Status Epilepticus in Adults

Status: 5 minutes of persistent seizures or >2 recurrent seizures without return to baseline
Non-convulsive Status: prolonged postictal state; odd behaviors (blinking, abnormal eye movements), 14% of convulsive seizures convert to NCSE

1/10 with SE does not survive to hospital discharge.

Causes of Provoked Seizures: Tumor/structural brain lesion, TBI, Alcohol (intoxication/withdrawal), Metabolic, Toxicologic, Pregnancy (eclampsia), Infection, HTN encephalopathy, Heat stroke.

INH OD: Give pyridoxine (mainly board review).
Workup: Sodium, Glucose, Calcium, Pregnancy test. EKG. CT brain with trauma, refractory seizure, antiacogulants, first time seizure. LP (immunocompromise or fever).

Always check glucose.

Decrease time to getting medications on board.

#1. Benzo: Lorazepam 4mg/Diazepam 5mg/Midazolam 10mg – usually 0.1mg/kg except for Diazepam which is 02.mg/kg.

RAMPART: IM Midaz (10mg) vs IV Loraz (4mg): 73.4% vs 63.4%. Time to treatment was 1.2min vs 4.8min.

#2. Phenytoin + Valproic Acid. Fosphenytoin: Loading dose 18-20mg/kg. Must give weight based dose. Valproic is also 20-40mkg/kg.

Usually after first 2 agents, usually refractory – intubate and needs continuous EEG.

#3. The Others (likely intubate).
Keppra: 1500mg loading. Phenobarbital 20mg/kg.
IV Propofol 1-2mg/kg then 1-15mg/kg/h.

#4 Pentobarb. 5mg/kg; likely need pressors.

#5 ??? Ketamine with benzos, Magnesium sulfate, Lacosamide, Hypothermia.


Status Epilepticus – Danya Khoujah, The 2015 Crashing Patient Conference 2015 – http://cloud.emedhome.com/cme/cme_45770_hi.mp4?iframe=true&width=920&height=470

165. Seizures and Status Epilepticus in Adults

163. Ataxia and Gait Disturbances


Failure to produce smooth intentional movements.  Is either sensory abnormality (due to peripheral nerves, spinal cord, or cerebellar input tracts) or motor abnormality (cerebellum).

Always walk your patient if you can with any neuro complaint.

Rapid thigh-slapping test: examines for dysdiadochokinesia or clumsy rapid movements. Have patient slap thigh with palm and then the back of the hand rapidly as fast as possible. Looks for lateral cerebellum dysfunction.

Finger-to-nose test: helpful for distingushing between cerebellar and posterior column (proprioception) by having them close their eyes (proprioception).

Heel-to-shin test: Cerebellar function in the lower extremities.

Stewart-Holmes rebound sign: sudden release of the flexed forearm, the individual fails to check the movement.

Romberg Test: standing with arms outstretched and eyes open. Look for unsteadiness – if present, has some ataxia. Have them close their eyes while doing it – if theres a large change in unsteadiness, romberg sign positive and suggests sensory ataxia such as posterior column/vestibular dysfunction or peripheral neuropathy.

Differential Diagnosis

Systemic disorders: intoxication with diminished alertness (alcohol, sedative-hypnotics), intoxication with preserved alertness (phenytoin, carbamazepine, valproic acid, heavy metals), metabolic disorders (hyponatremia, wernicke’s disease).

Local CNS disorders: cerebellum (hemorrhage, infarction, degenerative changes, abscess), cortex (frontal tumor, hemorrhage or trauma, hydrocephalus), subcortical (thalamic infarction or hemorrhage, parkinson’s disease, NPH), spinal cord (cervical spondylosis, posterior column disorders).

Peripheral Nervous System disorders: peripheral neuropathy (B12, folate), vestibulopathy.

Ataxia in Children

Drug Ingestion: Ethanol, phenytoin, carbamazapine, sedatives, lead, mercury.

Idiopathic: acute cerebellar ataxia of childhood (post infectious demyelinating disorder with onset of gait ataxia, occasional fever).

Infection and Inflammation: Varicella, Coxsackervirus A/B, Mycoplasma, Echovirus, Postinfectious Inflammation, Postimmunization.

Neoplasm: Neuroblastoma, CNS tumor.

Paraneoplasm: Opsoclonus-myclonus syndrome.

Trauma: SDH or EDH.

Congential or herediatry: Pyruvate decarboxylas deficiency, Friedreich’s ataxia, Hartnup disease.

Others: hydrocephalus, cerebellar abscess, labyrinithis, vestibular neuronitis, transverse myositis, meningoencephalitis.


Tintinalli, Chapter 163: Ataxia and Gait Disturbances

163. Ataxia and Gait Disturbances

162. Altered Mental Status and Coma


Acute confusion state, impairment of attention and cognition. Confusion can fluctuate. 4 general causes: intracranial disease, systemic disease, exogenous toxins, drug withdrawal. Alertness is reduced by difficulty maintaining attention and concentration. Sometimes drowsy, but generally awake. Sleep-wake cycle affected, causing ‘sundowning.’ Agitation can be treated with Halidol 5-10mg PO, IM, IV, though in elderly, may just start with 1-2mg. Benzos such as lorazepam/Ativan 0.5-2mg PO, IM, IV. Atypical antipsychotics are usually withheld in elderly due to increased mortality.

Infectious: pneumonia, UTI, meningitis/encephalitis, sepsis. Metabolic/toxic: Hypoglycemia, alcohol ingestion, electrolyte abnormality, hepatic encephalopathy thyroid disorders, drug withdrawal. Neurologic: stroke/TIA, seizure/post-ictal state, SAH, ICH, CNS mass lesion, SDH. Cardiopulmonary: CHF, MI, PE, hypoxia/CO2 narcosis. Drug-related: anticholinergic, alcohol/drug withdrawal, sedative-hypnotic, narcotic analgesic, polypharmacy.


Impairment of memory, particularly recent. Preservation of motor and speech abilities. Early: memory loss, naming problems, forgetting items. Middle: loss of reading, decreased performance in social situations, loss of direction. Late: extreme disorientation, inabilty to perform self-care tasks, personality changes.

Alzheimer’s: most common, still unknown etiology, thought to be related to amyloid deposits.

Vascular Dementia: second most common, CV disease with multiple infarcts. Sometimes have specific dates of worsening. Usually within 3 months of CV event or abrupt deterioration in memory or cognitive abilities.

Huntingtons: autodominant dementia.

Parkinson’s: increased motor tone, extrapyramidal signs of rigidity or movement disorders.

Vitamin deficiencies: consider checking B12 or folate.

Normal Pressure Hydrocephalus: Large ventricles on CT. Wet (urinary incontinence), Wobbly (ataxia, gait disturbance), and Weird (dementia). Consider trial of LPs or VP shunt to help improve symptoms.


Patient cannot be aroused. Function of the brainstem or both hemispheres altered to cause coma.

Uncal Herniation: use to medial temporal lobe shift onto brainstem. Drowsiness leading to ipsilateral slugginess to dilated nonreactive pupil. Ipsilateral hemiparesis.

CPP: Cerebral Perfusion Pressure: MAP (Mean Arterial Pressure) – ICP (Intracranial Pressure). If ICP approaches MAP, cerebral blow flow decreases and ischemia occurs.

Cushing Reflex: Due to increased ICP causing coma, hypertension and bradycardia.

Nonconvulsive status epilepticus: occurs with patient that had generalized seizure and remains unresponsive 30 minutes after seizure. In state of electrical seizure.

References / Resources

Tintinalli, Chapter 162: Altered Mental Status and Coma


Unedited Notes:

Coma is the dysfunction of arousal and awareness. Its a spectrum from brain death to minimally responsive.

Coma: eyes closed; reflexive, nonpurposeful or absent responsiveness.

Primary survey: airway protection, possibility of spinal injury, fingerstick, naloxone.

Neuro Assessment: LOC, Brainstem exam, motor function, breath pattern.

LOC: Spontaneous eye opening, visual fixation or pursuit, spontaneous and purposeful movements.

Coma Scales

GCS vs FOUR score. FOUR score: Eye response (0-4), Motor Response (0-4), Brainstem reflexes (0-4), Respiration (0-4). – Came out around 2005. Trying to assess brainstem function unlike GCS.

Brainstem exam: pupillary light reflex, corneal reflex, visual threat reflex, oculocephalic reflex, gag/cough reflex.

Motor function: assess response to proximal stimuli before distal stimuli. Assess proximally to sort out flexing vs withdrawing.

Structural Causes: Traumatic (ICH, SDH), neurovascular, neoplastic, AIDS related).

Metabolic Causes: Anoxi-ischemic, seizures, metabolic alterations, endocrinopathies, infections, OD, intoxications.


Approach to the Comatose Patient, Wendy Chang, The Crashing Patient Conference 2015 – http://cloud.emedhome.com/cme/cme_45769_hi.mp4?iframe=true&width=920&height=470

Intracranial HTN does not equal herniation. Its a spectrum.

Uncal herniation: medial portion of temple lobe goes downward into tentorium: ipsalateral pupil dilation, contralateral limb weakness.

Subthalsine heration: contralateral lower extremity weakness. Decreased LOC as well.

Tonsillar hernation: cerebellar parenchyma pushingdown into forumen magnum. Most rapid decline.

GCS drop in 2 points + anisocoria + posturing: diagnosis of herniation until proven otherwise.

Pupillary dilation localizes herniation better than limb weakness.

Treatment: Reducing blood volume: avoid hyperemia, remove clot/mass. Reducing CSF Volume: shunts/drains; Reducing cerebral ischemia: analgesia/sedation, induce pharm coma, induce hypothermia.

Tier 0: elevated head of bed, avoid neck constriction, treat fever/pain/agitation.

Tier 1: CSF draingage via ventriculostomy, hyperosmolar therapy (mannitol vs hypertonic saline).

Tier 2: additonal hyperosmolar therapy, sedation with propofol.

Tier 3: induce pharma coma (barbituates), induce hypothermia.

Intracranial Hypertension and Herniation, Yemi Adebayo, The Crashing Patient Conference 2015.


162. Altered Mental Status and Coma

161. Stroke, Transient Ischemic Attack, and Cervical Artery Dissection

Stroke Scale

NIHSS (National Institutes of Health Stroke Scale, 15 item, 0-42 score)

1a. Level of Consciousness: 0 – alert, 1 – not alert, but responds to mild stimuli, 2 – not alert, requires significant stimuli, 3 – only reflex motor, flaccid.

1b. LOC questions: Ask month and patient’s age: 0 – answers both, 1 – answers 1 correctly, 2 – answers both incorrectly.

1c. LOC commands: ask them to open/close eyes and grip/release hand: 0 – performs both, 1 – performs 1 correctly, 2 – performs neither.

2. Best Gaze: Only horizontal eye movements are tested. 0 – normal, 1 – partial gaze palsy, pt able to deviate away from gaze, 2 – forced gaze, unable to break it.

3. Visual: visual fields tested. 0 – no vision loss, 1 – partial hemianopsia, 2 – complete hemianopsia (half of vision on both eyes gone), 3 – bilateral hemianopia (blind).

4. Facial Palsy: show teeth and raise eyebrows/close eyes. 0 – normal symmetry, 1 – minor paralysis, 2 – total or near paralysis, 3 – complete paralysis of one/both sides – no movement of facial muscles at all.

5. Motor Arm: raise limp palms down for 10 seconds. 5a and 5b (left/right). 0 – no drift, 1 – drift eventually before 10s, 2 – some effort, but limb cannot get to fun 90 degrees, 3 – no effort against gravity, 4 – no movement.

6. Motor Leg: raise leg to 30 degrees for 5 seconds. 6a/6b (left/right). Same as Motor Arm.

7. Limb Ataxia: finger to nose and heel-shin test on both sides. Tests of unilateral cerebellar lesion. 0 – None. 1 – Present in 1 limb. 2 – present in two limbs (assuming both arm and leg).

8. Sensory: you can test as many spots as possible to get a better score. 0 – no sensory loss, 1 – mild to moderate sensory loss, 2 – severe to total sensory loss, patient not aware of being touched.

9. Best Language: Describe what is happening in picture (mother with cookies and overflowing water). 0 – no aphasia, 1 – mild-to-moderate aphasia – some obvious loss of fluency/facility of comprehension, 2 – severe aphasia, very fragmented expression, lots of guessing by listener, 3 – mute, global aphasia.

10. Dysarthria: read or repeat words. 0 – normal, 1 – mild to moderate dysarthria, slurs at least some of the words, 2 – severe dysarthria, speech is so slurred its hard to comprehend.

11. Extinction and Attention: Looking for neglect. 0 – none, 1 – visual, tactile, auditory, personal inattention to bilateral simultaneous stimuli, 2 – profound heme-attention or extinction.

Stroke Types

Ischemic: 87% of all strokes, 3 types: thrombotic (sometimes waxing and waning prior to stroke, common cause of TIA), embolic (usually sudden onset, only 20% of ischemic strokes), and hypoperfusion (usually cardiac failure).

Hemorrhagic: intracerebral (10% of all strokes) and nontraumatic SAH (3% of all strokes). Usually sudden onset as well.

Anterior Cerebral Artery Infarctions: uncommon, contralateral sensory/motor in the lower extremity with hand/face sparing. If on right leg, sometimes akinetic mutism (unable to speak) where as on left leg, confusion or motor hemineglect can be apparent.

Middle Cerebral Artery Infarctions: most common, since left hemisphere is usually dominant (in all right handed people and 80% of left handed people), aphasia usually with right sided weakness where as inattention/neglect, dysarthria would be left sided weakness. Deficits in face/upper extremity more than lower. A homonymous hemianopsia and gaze preference toward the side of the lesion can be seen regardless of the side of the lesion.

Posterior Cerebral Artery Infarctions: visual field defects (contralateral homonymous hemianopsia and unilateral cortical blindness), most common symptom though is unilateral headache. Light touch and pinprick deficits, alexia (unable to read), inability to name colors, recent memory loss. Motor deficits are minimal.

Vertebrobasiliar Infarctions: multiple simultaneous symptoms: usually vertigo, headache, nausea, visual disturbances, oculomotor disturbances, ataxia. Hallmark of posterior circulation stroke is crossed neuro disorders (ipsilateral CN deficits with contralateral motor).

Basilar Artery Infarctions: severe coma, quadriplegia, locked-in syndrome. Due to pontine tectum lesions – complete muscle paralysis except for upward gaze.

Cerebellar Infarctions: vertigo, gait instability, limb ataxia, headache, dysarthria, nausea/vomting, CN abnormalities. CT of posterior fossa artifact usually not accurate so usually needs MRI or MRA. Looking for obstructing hydrocephalus – would need emergent NSGY consult.

Lacunar Infactions: pure motor or sensory deficits.

Cervical Artery Dissection: 10-20% of all strokes in patients young and middle-aged. Peaks at 5th decade. Risks: history of neck trauma (major or trivial), family history or genetic factors, recent respiratory infections, hx/o migraines or connective tissue disorder. Both anterior and posterior can cause transient/persistent symptoms. Anterior (internal carotid) symptom generally is unilateral anterior headache or neck pain. Usually frontotemporal though can be varied. Partial Horners has been linked. Vertebral artery dissection usually presents with posterior neck pain and occipital headache as well as unilateral facial paresthesia, dizziness, vertigo, nausea/vomiting, diplopia, ataxia, limb weakness, numbness, dysarthria, hearing loss. Median time between neck pain and neuro symptoms is 14 days. MRI/MRA and CT/CTA are the way to check for it.

Stroke Management/Treatment

General Management: ABCs, IV access, bedside glucose, check Hgb, platelets, pulse ox, ECG, CT noncontrast, cardiac enzymes, strict bedrest with head of bed to 30 degrees.

Hypertension: If patient not candidate for tPa, permissive hypertension with no active attempts to lower BP unless SBP > 220 or diastolic BP is > 120. If going to reduce, reduce only 10-25%. If receiving or had received tPa, need to keep SBP < 185 or DBP < 110. Use Labetolol 10-20mg IV over 1-2min, may repeat x 1 (prior to receiving tPa though if already received, can go up to 300mg total) or nitro paste 1-2inch (C/I with viagra), nicardipine infusion (5mg/h, can increase by 2.5 up to max 15mg/h.

NINDS: 1996 trial, tPa within 3 hours. Only 624 pts, showed no difference in treatment at 24 hours, though did show favorable outcome at 3 months. Symptomatic ICH occurred in 6.4% compared to 0.6% in placebo.

ECASS (European Cooperative Acute Stroke Study III): expanded upon NINDS to tPa treatment within 3-4.5hr in 18-80yos. AHA/ASA endorsed it, but FDA has not approved it.

tPa: 0.9mg/kg, max dose of 90mg, 10% bolus, rest remaining over 60 minutes. No anticoagulation/antiplatelets given in first 24 hours. NINDS exclusion: SAH concerns, initial seizure, previous head trauma or stroke within last 3 months, previous MI in last 3 months, previous GI/GU hemorrhage in last 3 weeks, major surgery in last 2 weeks, prior ICH, SBP > 185/DBP > 110, active bleeding or acute major fracture, glucose < 50, INR > 1.7, use of heparin recently with elevated PT, Platelets < 100. Needs ICU admission if received for neuro checks, looking for possible side effect of angioedema as well.

Antiplatelet Therapy: Dipyridamole + Aspirin after TIA showed possible better benefit; still well received to just start aspirin only after TIA, though can consider plavix if already on aspirin. After acute stroke, 324mg aspirin should be started within 24-48hrs after.

Warfarin/Coumadin: Atrial fibrillation with acute stroke: increased risk of hemorrhagic conversion so consensus is to withhold heparin/lovenox/warfarin initially and have it started while in the hospital, but not in the ED.

Hemorrhage Stroke Treatment: If ICP elevation suspected, head of bed up 30 degrees, head midline, analgesics/sedation, osmotic therapy with mannitol vs hypertonic saline, mild hyperventilation, barb coma.

Cervical Artery Dissection: treated with IV heparin with conversion to warfarin.

TIA (Transient Ischemic Attack)

Transient episode of neuro dysfunction without acute infarction. Typically less than 1-2 hours, should be considered to be like unstable angina. 90-day overall stroke risk after TIA is > 10%, 50% of subsequent events occurred within 2 days.

ABCD2: risk stratify low-risk patients for possible outpatient workup for TIA. Varied results from external validity still showing increased risk with even the low risk group. A – Age > 60, B – BP > 140, C – Clinical Features: 1- Speech Impairment, 2 – unilateral weakness, D – Duration: 1 – 10-60 min, 2 – > 60 min, D – Diabetes. Low Risk is 0-3, Moderate 4-5, High 6-7.

References / Resources

Tintinalli, Chapter 161 – Stroke, Transient Ischemic Attack, and Cervical Artery Dissection

NIHSS Video Tutorial/Simulation – FREE 3.0 CME Hours


Unedited Notes:

Acute Stroke is clinical diagnosis. Sudden onset of neuro deficits explained by vascular cause.

Glucose is the only absolute requirement before tPa lab wise. If on anticoagulants coumadin, need INR or if considering platelet issue, then need that checked otherwise. No labs required.

CT brain noncontrast is only needed.

Early signs of infarction (blurry of gray/white), hyperdense MCA sign – can be candidate for endovascular repair).

Needs BP less than 185/110

Exclusion criteria: basically risk factors for patient bleeding bad if got tPa (head trauma or prior stroke in less 3 months, concerns for SAH, previous ICH, intracranial neoplasm/AV malformation, aneurysm, intracranial or intraspinal surgery, active internal bleeding, acute bleeding diathesis, platelet < 100, Heparin within last 48 hours, INR > 1.7, current use of direct thrombin inhibitors or direct factor Xa inhibitor, glucose < 50, CT shows hypodensity > 1/3.

Seizure is no longer in exclusive criteria (though it is relative C/I, minor).

3-4.5 window exclusions: > 80, severe stroke (NIHSS>25), taking oral anticoagulant, hx/o DM and prior stroke.

Use short acting titratable IV agents: labetolol, nicardipine, clevidipine.

If not candidates, perimissive HTN up to 220.

tPa (0.9mg/kg – max 90), 10% over 1 min, remainder over 1 hour.

Risk of ICH with tPa: NIHSS 0-10 2-4%, 11-20 4-5%, >20 17%. ECASS 7.9%. 6.4% for NINDS total.

Endovascular treatment:

IV tPa: ICA-T: 4-8%, MCA-M1 24-32%, MCA-M2: 31-44%. Sometimes clot is too big.

SYNTHESIS/IMSII/MR RESCUE – first generation. Achieved recanalization at 25-41%, no clinical benefit.

MR CLEAN/ESCAPE/SWIFT/PRIME/EXTEND IA/REVASCAT – used stent retrievers, recanalization at 59-88%, all showed clinical benefit.

2015 AHA/ASA Update: Meet all following criteria: prestroke mRS score 0-1, acute ischemic stroke receiving IV tPA within 4.5 hours according to regular guidelines, causative occlusion of ICA or proximal MCA M1 (hyperdense MCA, CTA (best way), angio if high suspicion, MRI), age > 18, NIHSS > 6, ASPECTS > 6 (Alberta Stroke Program Early CT score – don’t want to repervuse brain that’s already dead – , Tx can be initiated (groin puncture) within 6 hours of symptom onset.

Deterioration after tPa: 6-8 units of cryoprecipitate, 6-8 units of platelets, consider 40-80 ug/kg of rFVII – depends on circumstances.

Noncontrast CT: sensitive for acute hemorrhage.
MRI: Gradient echo, T2 susceptibility weighted, and FLAIR MRI are as sensitive for detection of acute blood, more sensitive for prior hemorrhage (more in T2W and GRE).

Acute ischemic present? 4-60% for 6-hour time window.
NCCT: insular ribbon sign (hyperdense vessel), basal ganglia sign (make out internal capsule, thalasmus – should be able to make out demarkation of lines) loss of gray-white differentiation.

DWMRI (measures net movement of water in tissue): accurate within minutes. To differenitae acute from subacute, DWI is used with conjunction with older MRI modalities.

Posterior fossa: NCCT terrible at seeing ischemic stroke. DWMRI better.
Posterior fossa stroke: misses posterior circulation ischemia up to 20% of the time. Can’t completely rely on it.

CTA: covers entire brain, can assess carotid/vertebrobasiliar system, sensitive for detection of IC aneurysms > 4mm. Helps show the collaterals. If you’re looking for aneurysm > 4mm, its 100% sensitive. Pro CT/LP: aneurysm < 4mm can rupture, CTA diagnoses the potential cause, not the hemorrhage itself. CTA will not diagnosis meningitis, IIH, or CVST (venous sinus thrombosis).

Salvageable brain tissue

Infarction (dead, not coming back) vs penumbra (hypoperfusion, likely ready to die) vs benign oligemia (hypoperfused, though likely not going to die).

Core Infarct: NCCT normal, DWMRI sees it.
CT Perfusion: inject dye, and tracts dye as it goes thru brain parenchyma. Allows quantitative assessment of CBV and CBV. Tech dependent. Scan thru in rapidedly. Radiation dose is higher. CT Perfusion only get 4 slices of brain – doesn’t do the whole brain.
MTT: Artery to Vein Mean Transit Time. Looking for mismatched. – able to see areas of hypoperfusion – might need intervention. Does this mean all the areas that would die without intervention – unsure of this at this time (could be benign oligemia though). Sort of like a VQ scan. You can get close to same radiation for NCCT for CTP with the correct settings.

LA Motor Scale: used to find big, meanful strokes. 3 things: facial droop, arm drift, grip strength.

MR-CLEAN: tPa alone vs mechanical/IA + tPa (most, not all). Median time from time of onset to tPa was 88 minutes. Groin puncture at 260 minutes ( 4-5 hrs) median time in 84%. Ideally cath lab by 4.5 hrs.

IMS-3: Similar to MR-CLEAN. Better outcomes in tPa + cath lab.

ED and Early Management of Large Vessel Occlusion, William Meurer, 2016 MCEP Critical Care in the ED, eMedHome.


161. Stroke, Transient Ischemic Attack, and Cervical Artery Dissection

160. Spontaneous Subarachnoid and Intracerebral Hemorrhage

Subarachnoid Hemorrhage

Risk Factors: HTN, smoking, alcoholics, polycystic kidney disease, family history of SAH, marfan/ehlers-danlos syndrome, coarctation of aorta.

Features: Acute onset within a few minutes, ‘thunderclap,’ previous history of similar headaches recently (sentinel bleed), 20% develop symptoms after exertion (exercise, sexual activity, defecation). Syncope alone should not raise suspicion for SAH.

Diagnosis: Noncontrast CT has same sensitivity if not better than MRI for blood. Better sensivity the earlier the CT is done. CSF analysis is still considered ‘gold standard’ after negative CT despite newer studies pointing against this. Two CSF tests: xanthochromia and RBC count.  It takes 12 hours to develop xanthochromia and remains present for almost 3 weeks. Traumatic LP results are still inconclusive and there is no general consensus on what number means true SAH. Generally, < 5 is definite no blood. CTA does not entirely rule out SAH (20% will have no aneurysm) and does not rule in SAH when aneurysm found (small % in population will be found incidentally).

Classification: Hunt-Hess Scale: I – mild headache, normal neuro exam; 2 – severe headache, normal neuro exam, may have CN deficit; 3 – confused, somnolent, may have CN deficit or mild neuro deficit; 4 – stupor, moderate to severe motor deficit, intermittent posturing; 5 – coma, reflex posturing or flaccid.

Treatment: Prevent complications: vasospasm (usually 2-21 days after, modest benefit with nimodipine 60mg PO q4), rebreeding (within first 24 hours, adequate BP control with MAP < 130mmHg, consider titratable labetolol), cerebral infarction, cerebral edema, hydrocephalus. 5-20% will have seizure – discuss with NSGY on need for prophylaxis.

Intracranial Hemorrhage

Risk Factors: 8-11% of all strokes, warfarin use, 3-9% of tPa use in ischemic stroke, long standing HTN, AV malformations, use of sympathomimetics (cocaine, phenylpropanolamine (decongestant).

Features: In hypertensive ICH, bleeding usually in putamen, thalamus, pons, or cerebellum (most common areas in ascending order).

Treatment: Management of elevated ICP: raise head of bed to 30 degrees, pain control/sedation, osmotic diuretics, mild hyperventilation with intubation. BP control if MAP > 150 or SBP > 180. Coagulopathy needs to be reversed. Warfarin reversal: Recombinant Factor VIIa or PCCs are mainstream now compared to FFP. Still need to add on Vitamin K, though slower.


Tintinalli, Chapter 160: Spontaneous Subarachnoid and Intracerebral Hemorrhage

Intracerebral Hemorrhage, Mike Abraham, The Crashing Patient Conference 2015

Subarachnoid Hemorrhage, Gunjan Parikh, The Crashing Patient Conference 2015

Unedited Notes:


Etiology of ICH: chronic HTN, cerebral amyloid agiopathy, sympathomimetics/cocaines, AVM, other vascular malformation.

Volume is a better predictor of morbidity than location.

Supratentorial: basal ganglia, lobar; infratentorial: pons, cerebellum; intraventricular involvement.

Calculate ABC/2 score. Calculate volume by taking the largest diameter, multiplying that by the total slices the bleed goes thru (0.5cm slices and on 6 slices would mean 3cm), then divide by 2 to get approximate volume.

ICH score: GCS, ICH volume, IVH, location, age: higher the number, the worse the prognosis. Score 6: 99% 30day mortality.

Main treatments: Look at BP and look at coagulopathy.

BP control: get SBP to 140, nicardipine/labetolol, try to achieve in 1 hour.

Coumadin: Vitamin K, give FFP. If C/I (hx/o CHF) to FFP, given PCCs.

Heparin: Protamine.

Antiplatelets: consider platelet transfusion, consider DDAVP.

Direct thrombin inhibitors: FFP, PCC, protamine. No improved outcomes any better even if the numbers look better in the studies.

Factor Xa inhibitors: FEIBA, dialysis. Antidote just approved. Outcomes still not that promising even if numbers are.

Secondary Treatment:

Seizures: routine prophylaxis not recommended. Treat all seizures aggressively if present. Continuous EEG monitoring may be helpful. Usually start with keppra (1-1.5g bolus).


CT scan: Thick blood in the cisterns. Sellate appearance of thick blood.

12-15% die before they reach the hospital. 50% survivors have persistent neuro deficits.

Females > males. Median age in the 50s.

Features: worst headache of life, neck pain/stifness, LOC (due to increased ICH at maximal on first rupture with brief loss of blood flow to the brain), nausea/vomiting.

Hunt and Hess Grading Scale. Grade 1-5.

Hunt and Hess Scale

EKG findings: peaked T, ST changes, Takosubos cardiomyopathy (contraction band necrosis, apical ballooning on echo).

Can be increased ICH during intubation: get everything right and get sedation/pain medications on early to prevent major changes in SBP. Use nicardipine for BP as well.

CT sensitivitiy drops over time. 98-100% within 12 hours.

CSF: Xanthochromia is present (minimal clearing of RBCs between tubes 1-4 (not completely valid either).

If CT positive, go ahead and get the CTA.

<20% have seizures. Guidelines recommend prophylaxis.

Worsening neuro decline: Rebleeding (number 1 cause), hydrocephalus, seizures cerebral edema, vasospasm (peak day 7) – nimodipine (not really necessary for ED), fever, hyponatremia.

SBP < 160, euvolemia. MAP > 70 or > 130 associated with poor outcome.


160. Spontaneous Subarachnoid and Intracerebral Hemorrhage