neurology

lecture given 5/11/2026

stroke

a neurologic event caused by interruption of oxygenated blood to the brain

ischemic- thrombotic and embolic

hemorrhagic- intracerebral and subarachnoid

ischemic strokes- thrombotic

clot forms in a narrowed blood vessel

risks include hyperlipidemia, HTN, diabetes, smoking, metabolic disorder

ischemic strokes- embolic

clot travels to a blood vessel in the brain

risks include atrial fib, valvular issues, atherosclerosis

how are ischemic strokes managed?

IV thrombolysis (TNK)- clot buster, medication given within 4.5 hrs of symptom onset, risk of bleeding complications increases as time passes

mechanical thrombectomy- endovascular procedure to remove blood clot, only certain clots are accessible (large vessel occlusions), can be done within 24 hrs in select pts, but essential to do as soon as possible

hemorrhagic strokes- intracerebral

often times hypertensive or secondary to an intracranial tumor

traumatic esp if on anticoagulation

hemorrhagic strokes- subarachnoid

often times an aneurysm wall weakens resulting in breakage

many complicaations including hydrocephalus, seizures, and vasospasams which can contribute to additional ischemic strokes

how are hemorrhagic strokes managed?

lower BP, reverse anticoagulation, if very large decompressive surgeries

subarachnoic hemorrhages from aneurysm ruptures require several days of ICU level of care given the high risk of complications

what is the clinical presentation of stroke?

left MCA: right arm/face/leg weakness, visual field loss on the right, aphasia

right MCA: left arm/face/leg weakness, visual field loss on the left, neglect to the left side

posterior circulation: vertigo, cranial nerve deficits, ataxia

left side of the brain controls ___ , while the right side controls____

right side of body and language

left side of the body and attention

what are signs of a stroke?

act FAST

face droops

arm weakness

speech difficulty

time is critical

what is given for ischemic stroke prevention?

antithrombotics- antiplatelet (aspirin/clopidogrel), given for small vessel disease / anticoagulants (warfarin, apixaban, rivaroxaban, dabigatran), given for a fib and heart failure

what are dental considerations for stroke pts?

due to neurologic deficits, their oral hygiene may suffer (hemi neglect, visual deficit, physical barriers)

may need medical clearance for certain dental work

medication interactions

dental caries and perio disease contributing to stroke

t/f you have to postpone dental care for 180 days after a pt has a stroke

false- research found no difference in risk of secondary stroke with dental work performed within 30-180 days

t/f you should have your pts on anticoagulants stop them before any proccedure you do

false- thrombosis risk outweights bleeding risk in may cases, speak to PCP when extracting multiple teeth

epilepsy

two unprovoked seizures OR one unprovoked seizure and a probability of future seizures on abnormal MRI or EEG

umbrella term for a large group of seizure disorders

just because someone has a seizure does not mean they have epilepsy

epileptic seizure

a transient occurance of signs and/or symptoms due to abnormal excessive or synchronous neuronal activity in the brain

focal seizure

onset involved one brain region

generalize epileptic seizure

onset involves bilateral brain hemispheres

unknown epileptic seizure

unclear onset of seizure

what is the natural progression of a seizure?

aura- sensory changes or deja vu prior to an event

ictal period- seizure

post ictal period- fatigue, confusion (may last several hours)

how are seizures medically managed?

medical management can prevent seizures occurrance but don’t impact the underlying disease process

antiseizure meds reduce risk recurrance from 50-35% in pts at medium risk

up to 40% of newly diagnosed epilepsy patients may have drug resistant epilepsy

t/f seizures can be managed surgically via resective surgery or neuromodulation

true

are seizures dangerous?

yes- if status epilepticus (>5min seizure) remains untreated, hyperexcitability of neurons can result in futher damage to the brain

sudden unexpected death in epilepsy

trauma, drowning

what are precautions for seizures?

no driving until 6mo of being seizure free

no swimming/bathing alone

no operating heavy machinery, climbing ladders, ect

what are comorbidities with epilepsy?

23% have active depression, cognitive difficulties, psychiatric comorbidities

convulsive syncope

fainting that leads to convulsions

can distinguish from seizure by identifying clear trigger, prodrome, limb/loss of consciousness followed by convulsions, and rapid improvement with lying down and return to self with no post-ictal confusion

psychogenic non-epileptic seizures

seizures that do not hvae an EEF correlate and are thought to be a stress response

10-30% of patients have epileptic seizures

treatment is CBT

same precautions as epileptic seizures

what are dental considerations for epileptic pts?

anti-epileptic drugs and their side effects, traumatic injuries secondary to seizures, seizure during dental visit

what are some anticonvulsants that have dental implications?

phenytoin, carbamazepine, valproic acid, lamotrigine, levtiracetam

what should you do if a pt has a seizure in a dental chair?

remain calm, protect pt from injury, no further dental treatment, if prolonged seizure use lorazepam 2mg if available and transfer to ED

parkinson’s disease

a progressive degerative disorder that results form loss of dopamine producing neurons

increasing prevalence with time, affecting >2% of the population over 65 yrs

hereditary, environmental, sporadic

what is the clinical presentation of parkinson’s disease?

resting tremor, slow movements, rigidity, masked faces, orthostatic hypotension, constipation, dementia (later onset)

what are diagnostics for parkinson’s?

DAT scan evaluating degree of dopamine uptake within the brain (abnormal is low uptake)

skin biopsy evaluating for alpha synuclein (misfolds forming lewy bodiess)

clinically and/or empiric treatment trial

does parkinsonian features mean the pt has parkinson’s?

no- common mimics are antipsychotic medication side effects, mood disorders resulting in psychomotor slowing, multi-system atrophy, other tremors (essential, physiologic, ect)

what medications are given for parkinson’s disease?

carbidopa/levodopa, dopamine agonists, dopamine relase, MAO B inhibitiors, COMT inhibitors

how can parkinson’s disease be managed surgically?

deep brain stimulation- device inserted by neurosurgery that allows modulation of dopaminergic pathways

can help improve pts with tremor and bradykinesia, not so much freezing/gait

what are dental considerations for pts with parkinson’s?

minimize poor dental outcomes that results from motor deficits, avoid drug interactions

oral hygiene- frequent preventative care visits, collis curve toothbrush and mechanical toothbrushes, chlorohexidine rinses, topical fluoride, appointments timed during the day when they have minimal on/off fluctuations

alzheimer’s disease

neurodegenerative disease caused by amyloid plaques and neurofibrillary tangles

accumulates most commonly in medial temporal lobe and cortex

short term recall impairment, executive function/language/behavioral changes

stages: preclinical/presymptomatic, mild or early, moderate, severe or late stage

how is alzheimer’s diagnosed?

traditional imaging findings: temporal parietal atrophy, amyloid PET scans, neurocognitive testing

what are risk factors for alzheimer’s?

increasing age, genetics, head injuries, environmental

how is alzheimer’s managed?

social management: socialization, physical activity, assistance with ADL and iADLs

medical: donepezil, rivastgmine, dalantamine, memantine, lecanemab (targets amyloid plaques for clearance

what are dental considerations for pts with alzheimer’s?

frequent preventative visits

trigeminal neuralgia

episodic often unilateral attacks of brief stabbing pain in the distribution of the trigeminal nerve

common triggers include eating, brushing teeth, touching face, talking

classic- artery compresses nerve at its transition zone

secondary- compressive mass, MS

when to suspect trigeminal neuralgia vs dental pain?

episodic short bursts of stabbing pain, often able to identify a trigger, unremarkable dental exam

what are some medical/surgical interventions given for trigeminal neuralgia?

carbamazepine, oxcarbazepine, gabapentin, lamotrigine, depakote

microvascular decompression, radiofrequency thermal lesion, rhizotomy with chemical injection to damage the nerve

trigeminal autonomic cephalgias

trigeminal neuralgia with autonomic signs- lacrmination, rhinorrhea, miosis, ptosis

cluster, paroxysmal hemicrania, short lasting neuralgiform attacks (SUNA)/with conjunctival injection and tearing (SUNCT)

cluster headaches

1-2 attacks per day usually at the same time of day, often occurring in clusters

15-180 min long

abortive treatment- triptans, 100% O2

preventive treatment- prednisone burst, verapamil, lithium, antiepileptics

paroxysmal hemicrania

1-40 attacks a day

2-30 min long

treatment with indomethacin (responsive by definition)

SUNA/SUNCT

60-100 times per day

5-240 sec long

treatment with lamotrigine, gabapentin, topiramate

bell’s palsy

rapid unilateral onset of CN VII lower motor neuron dysfunction

25% of pts may have persistent moderate to severe facial asymmetry

can be anatomica (internal auditory canal size), viral or bacterial infection (HSV, lyme), ischemic, autoimmune

house-brackmann scoring

scoring for bell’s palsy, graded on scale of I to VI

mutliple sclerosis

autoimmune demyelinating disease of the CNS

risk factors of exposure to UV B radiation/vitamin D, genetics, EBV, smoking, obesity, microbiome, and diet

what are clinical symptoms of MS?

optic neuritis, focal neurologic deficits (symptoms depend on site of demyelination)

classifications- relapsing remitting, secondary progressive, primary progressive

how is MS diganosed?

MRI- round/ovoid lesions along periventricular, juxtacortical/cortex and spinal cord / optic nerve enhancement

CSF- signs of inflammation like elevated proteins, oligoclonal bands, and mild pleocytosis

how is MS treated?

relapses- high dose steroids to hasten recovery

disease modifying treatments- CD20 monoclonal antibodies, integrin inhibitor, fumarates, sphingosine-1 phosphate modulators, beta interferons

amyotrophy lateral sclerosis (ALS)

neurodegenerative process affecting motor neurons

acquired or hereditary (familiar or sporadic)

what is the clincial presentation of ALS?

bulbar onset- spastic or flaccid dysarthria, slow tongue movements, dysphagia

limb weakness

pseudobulbar affect

frontal temporal dementia

how is ALS diagnosed?

phsical examination demonstrating lower and upper motor neuron signs- hyperreflexia, muscle atrophy, tongue atrophy/fasciculations

electromyography (abnormal motor with normal sensory responses and findings of ongoing nerve damage)

how is ALS treated?

supportive- pulmonary, speech and swallow

riluzole, edaravone