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Define TIA.

Sudden focal neuro deficits that resolve within 24 hrs, no residual deficits, usually last 15 min


Describe the basic pathophysiology of a TIA.

Ischemia… followed by natural breakdown of blockage or collateral blood flow:
i. Atherosclerosis (enlarged atheroma most common cause) or small vessel dz (DM/HTN)
ii. Embolus
iii. Vasculitis


Describe the clinical presentation of a TIA arising from the:
- Carotid a.
- Basilar a./SCA/AICA
- Vertebral a./PICA

- Carotid a.--amaurosis fugax (transient monocular blindness) via ophthalmic a.

- MCA--transient hemiparesis, aphasias

- PCA--transient homonymous hemianopsia

- Basilar a./SCA/AICA--dizziness, dysphagia, dysarthria, diplopia, cerebellar ataxia

- Vertebral a./PICA--cerebellar ataxia, +/- medullary syndrome


What is the w/u for TIA?

MRI/MRA brain, carotid doppler, TTE/TEE, check glucose and BP control, if no yield--vasculitis autoimmune serum panel and LP for CSF analysis


What is the tx for TIA if atherosclerotic?

If Embolic?

If atherosclerotic: Start antiplatelet (ASA, or ASA+ clopidogrel (Plavix) common) + statin
1. Surgical approach: carotid endarterectomy, possibly ballooning/stenting
2. Prevention: control DM, HTN, HLD, smoking cessation

If embolic: start anticoagulation (heparin, warfarin, Factor X inhibitors, etc)


Describe the basic pathophysiology of intracranial hemorrhage, both deep and superficial.

- Deep hemorrhage: from small vessel, (lenticulostriate) rupture due to HTN (remember cocaine can cause transient cerebral HTN too)

- Superficial hemorrhage: from head trauma, possibly CT disorders

Blood -> Increased ICP -> Severe HA, LOC or impaired consciousness, focal neuro deficits


Both deep and superficial ICH can be compounded if patient is:

Taking anticoagulation meds


What is the general clinical presentation of ICH?
- What additionally might you see w/ deep? Superficial?

HA, LOC, focal neurodeficits

- Deep hemorrhage: basal ganglia or thalamic lesions so movement or sensory disorders
- Superficial: depends, sx as previously mentioned in TIA


What is the w/u for ICH?

CT non contrast looking for bright blood!!!, others CTA, MRI/MRA, CBC/CMP, check INR


What is the tx for ICH?

Manage underlying bleeding disorder if any, FFP and coag factors in some cases, neurosurg for coil/clip placement


What types of seizures does phenytoin (Dilantin) treat?

Complex partial seizures


What types of seizures does carbamazepine (Tegretol) treat?

(Recall, what additional thing can it be used for?)

Complex or simple partial seizures

(also trigeminal neuralgia)


What types of seizures does lamotrigine (Lamictal) treat?

(Recall, what additional thing can it be used for?)

Most seizures (generalized tonic-clonic, absence...)

(also BPD)


What types of seizures does valproate (Depakote) treat?

(Recall, what additional thing can it be used for?)

Most seizures (generalized tonic-clonic, absence...)

(also BPD)


What types of seizures does oxcarbazepine treat?

Simple or complex partial seizures


What types of seizures does levetiracetam (Keppra) treat?

Most seizures


What types of seizures does ethosuximide (Zarontin) treat?



What are some SE's of anticonvulsants? (we will go into more detail, just read)

Anticonvulsants may cause confusion, somnolence and ataxia at high serum levels and teratogenicity at minimal serum levels.


What AED's (anti-epileptic drugs) cause confusion/drowsiness/dizziness?

Phenytoin, carbamazepine, lamotrigine, valproate, oxcarbazepine, levetiracetam (ALL OF THEM)


What are the teratogenic effects of:
- Valproate (Depakote)?
- Lamotrigine (Lamictol) and carbamazepine (Tegretol)?
- Phenytoin (Dilantin)?

- Valproate: NTDs

- Lamotrigine and carbamazepine: oral/facial clefts

- Phenytoin: fetal hydrantoin syndrome: minor dysmorphic craniofacial features and limb defects including hypoplastic nails and distal phalanges


Describe this protocol for treating generalized status epilepticus.

First give lorazepam (Ativan) 0.1 mg/kg (4-8 mg) as an IV bolus, repeatable in 5-10 minutes if needed, followed by loading with either fosphenytoin 20 phenytoin equivalents (PE)/kg IV, no faster than 150 mg/min, or phenytoin 20 mg/kg IV, given in saline no faster than 50 mg/min.

(Give benzo, then if needed give AED)


What are the indications for an emergency LP?

List some additional, less emergent indications.

- Meningitis
- Encephalitis
- SAH (if no blood is detected by CT scan in the latter)

Also for:
- Demyelinating inflammatory disease
- Nl pressure hydrocephalus ("W/W/W")
- Pseudotumor cerebri (AKA idiopathic intracranial HTN)


What are the contraindications for emergent LP?

- Increased ICP!!! (Signs like papilledema, LOC, focal neuro deficits, asymmetry/shifts on CT) b/c of risk of brain herniation
- Coagulopathy (INR > 1.5 or platelets < 50,000, 6hrs from last heparin, 5 days from last clopidogrel).
- Spinal cord trauma
- Cardiorespiratory compromise
- Overlying skin lesion/infx


Explain how CSF levels of WBCs, protein, and glucose are altered in the following types of meningitis:
- Bacterial
- Viral
- Tuberculosis
- Fungus

- Bacterial: WBCs: 500-1000 (PMNs), ^ protein, v glucose

- Viral: WBCs: < 500 (lympho's), v/nl protein, nl glucose

- Tuberculosis: < 500 (lympho's), v protein, ^ glucose

- Fungus: < 500 (lympho's), v protein, ^ glucose


What type of organism usually causes encephalitis?

In encephalitis, the LP is similar to which type of meningitis infection? (state WBCs, protein, glucose)

Usually viral
- Viral: WBCs: < 500 (lympho's), v/nl protein, nl glucose


When would you do a low-volume LP for assessing SAH?

What would the fluid look like if positive?

If CT came back inconclusive

- Xanthochromic CSF w/SAME # RBCs in tubes 1 and 4


What is a "traumatic tap" on LP?

How would the result differ from that of a positive SAH LP?

A "traumatic tap" occurs if the needle inadvertently has entered an epidural vein during insertion.
- Traumatic tap will NOT be xanthochromic, and # of RBC’s will drop from tube 1 to 4


How do you treat impaired consciousness due to hypoglycemia?

Give sugar


How do you treat impaired consciousness due to hypothermia?

Rewarming (externally + trunk first, if necessary warm intraperitoneal lavage)


How do you treat impaired consciousness due to narcotics?

Naloxone (Narcan)


How do you treat impaired consciousness due to benzos?

Flumazenil (Romazicon) is controversial, supportive care is standard of care


Describe how IV ______________ can reduce edema or herniation from certain cerebral lesions (tumor, abscess or encephalitis) or spinal cord lesions (metastatic cord compression, myelitis), but primary tx directed at the underlying lesion must soon follow.


As described above, IV dex can temporarily reduce the edema surrounding tumors/abscess by suppressing the inflammatory response system


S/s of herpes encephalitis?

Aphasia, behavior change, memory change


How is herpes encephalitis dx'd?

MRI: bilateral/asymmetric involvement of frontal + temporal lobes


Pathophysiology of MS?

Describe the lesions and their location

Acquired immune-mediated CNS demyelination, w/ secondary axon loss
- White matter plaques in optic nerves, spinal cord, and brain w/ periventricular predominance (also juxtacortical, infratentorial, spinal cord, etc)


Describe the typical progression of MS.

Starts relapsing/remitting, later secondary progressive phase w/o full recovery between episodes


Describe the common clinical manifestations of MS.

- Most common initial sx involve optic nerves (optic neuritis, INO) or LE motor deficits
- Trigeminal neuralgia
(+) Lhermitte’s sign also common (electrical sensation that runs down the back and into the limbs)


What is required for dx of MS?

Explain the w/u?

Multiple s/s separated by space and time.

i. Get brain/spinal cord MRI, new/active lesions enhance w/contrast
ii. Oligoclonal bands in CSF (clones of Ab’s), increased Ig synthesis in CSF


What is the tx for MS?

No cure
i. High dose IV steroids for acute MS attacks
ii. Beta-interferon or Glatiramer acetate reduces severity/frequency of attacks, lessens future cumulative neuro-disability in some
iii. Dalfampridine (K-channel blocker) increases conduction speed, improves sx
iv. Natalizumab: AB that blocks T-cell adhesion molecules to prevent BBB penetration (rare PML)


Use abortive therapy for migraines if less than ____________ (time).

1-2 months


Name the abortive therapy tx's for migraines.

i. NSAIDs (Ibuprofen, Naproxen), Analgesics (Tylenol, ASA) for mild migraine

ii. Triptans (can be IM, helpful if pt also has N/V)

iii. Dihydroergotamine (injection, nasal spray)


Name some prophylactic migraine tx's.

i. Beta-blocker (Propanolol), CCB (Verapamil)

ii. TCA (amytriptyline)

iii. Anticonvulsants (Valproate, Gabapentin, Topiramate)


What receptor is implicated in all migraine tx's in some way?



What are the tx's for tension HA's?

NSAIDS, analgesics, TCA’s


What are the s/s of a HA due to increased ICP?

Sx: suddenly severe HA + seizure, syncope, coma, neck stiffness, N/V, or vision dimming


In cases of suspected increased ICP, what should be ordered urgently and why?

LP urgently to exclude meningitis, SAH
- Get CT first in setting of papilledema to r/o mass lesions (brain tumor, abscess, intraparenchymal hemorrhage) that could cause brainstem herniation


What is the tx for increased ICP?

Merchut doesn’t say?
- Mannitol, hypertonic saline to reduce edema; if there’s an aneurysm, clip or coil it. Craniotomy to relieve pressure


*Describe the evaluation of an acutely confused or demented patient, emphasizing reversible or treatable
causes, with particular attention to Alzheimer's dementia.

a. How would you evaluate degree of confusion/dementia?
b. What labs would you get to r/o reversible causes?
c. What scan would you order and in order to r/o what (4)?
d. What would you order in the presence of fever/HA?
e. What should you order if the pt is young?
f. If none of the above, what is the dx?

a. Mini-Mental State Exam (MMSE) to evaluate degree of confusion/dementia
b. CBC, chemistry profile, vitamin B12, and thyroid fxn test to look for reversible causes
c. MRI to r/o etiologies like chronic subdural hemorrhage, brain tumor/abscess, multiple infarctions, NPH
d. LP in setting of fever/HA + acute dementia (r/o meningitis)
e. Young pt + dementia -> HIV test
f. Alzheimer’s: Dx of exclusion. Usually nl bloodwork, non-specific atrophy of aging on MRI. Diagnosis relies heavily on observations of family/friends


What are the 2 major causes of peripheral neuropathy?

For both mono and poly, due to either demyelination or axonal degeneration (nerve injury)


What are some causes of peripheral neuropathy due to demyelination?

Explain axonal degeneration cause.

Demyelination: can be from focal compression (carpal tunnel), GBS, others

Wallerian degeneration: axons/myelin degenerate distal to crushing/penetrating focal


Are toximetabolic causes of peripheral polyneuropathies usually due to demyelination or degeneration?

Trick- toximetabolic causes of polyneuropathies almost always cause axonal degeneration, with secondary demyelination


W/r/t peripheral POLYneuropathies, describe how the numbness is distributed.
- Does it start proximal or distally?
- What are the other s/s would you see?

Most common types start distally and symmetrically w/ numbness/tingling and move proximally, can eventually be stocking and glove
- Atrophy/weakness starts later, also begins distally
- Early decrease/loss of reflexes


Common causes of peripheral mononeuropathies?

If you see multiple mononeuropathies, what types of things should you consider?

Mononeuropathies are usually due to obvious causes like trauma or common sites of compression (median nerve at the wrist, ulnar at the elbow, peroneal at the fibular head)

Multiple mononeuropathies can be d/t systemic illness like SLE, sarcoid, or leprosy


List the causes of non-acute polyneuropathy (peripheral).

What things should you look for in the H&P?

DM (most common)
- Can be metabolic, autoimmune, cancerous, infectious

Look for causes like: meds (chemo), neurotoxin exposure, alcoholism, family h/o of hereditary neuropathy


What test is useful identifying different types of peripheral neuropathies?

When would you order an additional sural nerve bx as well?

EMG can help identify the type of neuropathy

- If EMG + clinical picture suggests inflammatory, immune-mediated, or vasculitic cause, get sural nerve biopsy to confirm dx


i. How do you treat the chronic weakness a/w peripheral neuropathy?
ii. What 2 topical meds can be given for chronic neuropathic pain?
iii. What 2 other categories of meds can be given for neuropathic pain?

[Reverse causative agent if found (decompress nerves, optimal glycemic control in DM, etc)]
i. Braces/splints/cane/walker for chronic weakness
ii. Topical capsaicin or lidocaine patches for chronic neuropathic pain
iii. Anticonvulsants (gabapentin, pregabalin, carbamazepine), antidepressants (duloxetine, amitriptyline) are effective for neuropathic pain


Tx for trigeminal neuralgia?

Gabapentin or carbamazepine (prevent the nerve from misfiring and producing the shock-like pain.)


Tx for postherpetic neuralgia?

What secondary tx may also help?

In a reactivation of the VSV infection that remains dormant in the dorsal roots, acyclovir should be administered immediately to limit disease progression and the development of postherpetic neuralgia.
- Topical capsaicin (depletes substance P, a pain mediator) or lidocaine applied to the area has shown pain reduction for all neuropathic pain.


Radicular pain always indicates:

What are some scenarios where it develops?

- It's the only way that an entire dermatome can be painful all at once.

It often occurs in a shingles flare up or disc herniation.


What is the best tx for radiculopathy?

If you can't do this, what are some secondary tx's to decrease the pain?

Surgical removal of the inflammatory insult (if possible) is the best way to get rid of a radiculopathy.
- Otherwise, analgesics, anti-inflammatory meds (steroids), and nerve block procedures help decrease the pain.


How is polymyositis dx'd?

Largely clinical dx (proximal weakness), confirmed w/ EMG, muscle bx showing inflammatory cells amongst necrotic/regenerating m. fibers.


Tx for polymyositis?

Immunosuppression (corticosteroids)


How is MG dx'd?
- Which of these methods is the best way to dx it?

Largely clinical dx (ptosis, dysarthria, dysphagia, diplopia all common). Tensilon test (pretty outdated though). LOOK FOR THE AUTOANTIBODIES (best way to diagnose, anti-AChR).


Tx for MG? (3)

Immunosuppression (steroids), AChE inhibitors (pyridostigmine), thymectomy is very effective.


How is ALS dx'd?

Largely clinical dx (combined UMN+LMN, often unilateral to start off, purely motor deficits, fasciculations).


Tx for ALS? (1)

Not much of any treatment except riluzole (NMDA-R antag.).


How is myasthenic crisis dx'd?
- What can trigger it?

Dx'd s/p seeing profound weakness/quadriplegia and inability to speak, swallow or breathe in a patient with known MG.
- Can be triggered by acute stressors like severe infection.


How is myasthenic crisis treated?

Neuro emergency, admit to ICU, maintain on ventilator.
- Treat current infection, immunosuppression if indicated.


What is GBS?

How is GBS treated?

GBS: Ascending paralysis that can often involve diaphragm.

Neuro emergency, admit to ICU, maintain on ventilator. Give immunosuppression to curb autoimmune process..


What are spinal cord syndromes?

Spinal cord compression; acute myelitis


How can you tell if spinal cord syndromes like sc compression or acute myelitis are intramedullary vs extramedullary?
What basic things can you do to treat?

Evaluate UMN, LMN signs to localize. Evaluate dermatomal sparing to determine intramedullary (suspended sensory level, sacral sparing, etc) or extramedullary (sacral involvement) etiology. Remove cause of compression if possible.


Describe the basic pathophysiology of Parkinson dz (PD).

a. Progressive loss of dopaminergic neurons from SNc.
b. This means loss of direct pathway “stimulation” of the VL thalamus and increase in indirect pathway “inhibition” of the VL thalamus.


What are the sx of PD? (which emerges first?)

- Tremor (resting; pill-rolling)
- Rigidity (cogwheel)
- Akinesia/bradykinesia
- Postural instability

First sx emerge from asymmetric upper extremities.


What is seen on histology in PD?

Eosinophilic, cytoplasmic Lewy bodies seen in dopaminergic nn.


What is the best medication tx for PD?
List all of the other options.

Treatment involves increasing dopamine in the CNS. TOC: Levodopa + Carbidopa (Sinemet). [Levodopa converted to DA in PNS + CNS via DOPA decarboxylase. Carbidopa inhibits peripheral conversion to decrease SE's]

- COMT inhibitors: tolcapone, entacapone
- MAO-B inhibitor: selegiline
- Anticholinergics: trihexyphenidyl


What makes up the dx of (familial) essential tremor?

Postural and kinetic tremors without underlying neurological cause.


How is (familial) essential tremor treated?

- Beta-blockers (TOC)
- Barbiturates
- Booze


What do an EEG do?

Records brain waves, which are periodically firing electrical potentials from the summated synaptic activity of pyramidal neurons. May record brain wave slowing or irritable electrical activity over a focal area.


What are some uses for an EEG?
- What pattern is seen on absence seizures?
- What pattern is seen on CJD?

- Used on epileptic patients in the ICU to detect when they have seizures. (Only see epileptiform waves when there is seizure activity, may miss).
- Sleep studies: used to detect what the different levels of sleep the patient is achieving.
- Absence seizure: 3 Hz spike and slow wave electrical discharge.
- CJD = periodic sharp wave discharge.


What do an EMG do?

What 2 broad categories does it help distinguish?

Detects electrical activity and function of nerves. Used as diagnostic tests of nerve problems. Detects subtle neuropathic clinical signs with regards to a more precise localization of the nerve lesion and its severity that otherwise cannot be elicited on physical exam.

Helps to distinguish between neuropathy and myopathy.


Describe the neurological criteria for brain death. (there are at least 7 points)

What is the currently preferred confirmatory test for brain death and how/why?

a. Apparent cause should be known and must be of sufficient severity to account for the irreversible coma
b. Lack of neurological improvement despite adequate tx of any reversible causes of coma (drug intox, circulatory shock, hypothermia, metabolic/endocrine abnormalities)
c. Does not show any hint or suggestion of cerebral fcn
d. All CNs/brainstem reflexes must be absent
e. No spontaneous respirations
f. When the etiology is known and no reversible cause requires tx with no improvement over 6 hours (not a hard cut off, but rather generally accepted). Younger pts' brains can withstand anoxia for longer = extend cutoff depending on age.

RADIOISOTOPE BRAIN SCAN is the currently preferred confirmatory test for brain death as it demonstrates the absence of cerebral blood flow over a 10 min period.


What is something you should always do when undergoing supportive care for incurable neurologic conditions such as anoxic encephalopathy (chronic vegetative state), ALS, and end-stage dementia?



Supportive care for pts w/anoxic encephalopathy (chronic vegetative state)?

- Nutritional support
- Reduce potential for nosocomial infection
- Prophylaxis against venous thromboembolism and gastric stress ulceration.


Supportive care for pts w/ALS primarily concerns what function?
- If pts opt for death at home via this mechanism, what medication can be Rx'd to help?

- O2, CPAP, BiPAP mask. Aggressive = mechanical ventilation via trach tube.
- Many patients opt for death by respiratory failure or pneumonia at home...relief of anxiety of dyspnea = BENZOS.


Supportive care for end-stage dementia?

- Constantly monitor behavioral changes.
- Constantly address nutrition, dressing, hygiene.