FINAL - Neuro Flashcards
What are 6 functions of the frontal lobe of the brain?
-Voluntary motor control, learned motor skills, planned movement
-Expressive speech (contains Broca’s area)
-Personality, emotions, judgement, socialization, drive
-Working/ short term memory
-Complex problem solving
-Olfaction
What are the functions of the temporal lobe?
-Mediates auditory input and auditory memory integration
-Contains Wernicke’s area
-Spoken and body language interpretation
-Memory
-Facial recognition
What does the occipital lobe do?
Visual input and processing
Where is Broca’s area? What happens if it is injured
Frontal lobe
Injury to Broca’s area= expressive aphasia (understands the words, cannot produce the speech)
It helps me to remember- Broca > broken speech
What are some functions of the parietal lobe?
-Interprets sensory information
-Perception
-Spatial awareness
-Manipulating objects
-Spelling
-Receptive speech
-Taste
What does the cerebellum do?
Coordinates smooth mote activities, processes muscle position
Where is Wernicke’s area? What happens if it is injured
Temporal lobe
Injury to Wernicke’s= receptive aphasia (does not understand/ interpret the words, can speak fluently but non sensical
“Wacky wernickes” (speech makes no sense)
What brain lobe mediates precise motor control and learned motor skills?
Frontal
What brain lobe interprets sensory information and allows for spacial discrimination?
Parietal
What brain lobe mediates auditory input and recognizes faces?
Temporal lobe
What brain lobe is responsible for vision?
Occipital
Janice has a lesion in her frontal cortex. What deficits might you expect?
-Personality changes, problems with behaviour control, emotional lability
-Difficulty planning, organizing, solving complex problems?
-If Broca’s area is affected, expressive aphasia
Fred had a lesion in his parietal lobe. What deficits might you expect?
-Problems with spatial discrimination
-Perceptual changes
Karen has a lesion on her temporal lobe. What deficits might you expect?
Problems understanding speech or body language
Ken had a lesion on his occipital lobe. What deficits might you expect?
Blindness.
T/F It is important to thoroughly assess a patient with a suspected concussion to rule out a functional disturbance in brain function.
False. Concussions are a functional problem. We want to carefully assess the patient for a structural problem (i.e., brain contusion, bleed). Michaela has a great write up about this in the neuro weekly notes if you want a refresher.
Describe the progression of concussions symptoms
Acute onset
0-72 hours: Physical symptoms predominate (HA, dizziness, nausea)
7- 14 days: Cognitive symptoms dominate (feeling in a fog, memory problems, slow processing speed)
21+ days: Psychosocial/ somatic dominant symptoms (anxiety)
What are expected concussion symptoms?
Somatic: HA, sleep disturbance, n/v, dizziness, blurred vision, fatigue, impaired balance, photophobia, noise sensitivity
Cognitive: confusion, amnesia, attention impairment, reduced processing speed, drowsiness
Emotion/ behaviour: Impulsivity, irritability, depression
What are the alarm symptoms of concussion?
-Focal neuro deficits
-Vision loss
-Hemiparesis
-Limb weakness
-Stroke sx
-Worsening HA
-Worsening confusion
-Worsening lethargy
-Battle sign (bruising behind the ear)
-Racoon eyes
-Hemotypanum
-Seizure
-2+ episodes of vomiting
How is a concussion diagnosed?
Clinical dx
CT per NOC or Canadian CT head rules
T/F Kids can return to sports after concussion within 3 days if there was no LOC
False
Sarah’s notes: At LEAST 5 days for kids before returning to sport
Best practice would be completing a return to play plan
Gradual increase from mental rest, light walking, strenuous activity, sport, allowing at least 24 hours at each stage
Generally will take about 3-4 weeks depending on individual/ injury
Why are we so concerned about a kid stopping play after a head impact or following a return to play plan?
Repeat TBI when the brain is vulnerable can lead to life threatening cerebral edema (Second impact syndrome) or permanent impairment, death.
You see a patient in clinic for a concussion. What red flag teaching do you send them home with?
Seek emergent care if
-Worsening symptoms (worsening HA, confusion, lethargy)
-Vomit 2 or more times
-Vision loss
-Numbness or tingling in arms or legs, weakness in any limb
-Stroke symptoms
-Seizure
66 year old Mario comes into your clinic, GCS 15, after he fell off a step ladder and hit his head. Does he require imaging?
Per Canadian CT head rules- yes
-GCS 15, high risk for surgical intervention (age >65) , dangerous MOI
15 year old Sally comes in to the ED, GCS 15, following LOC x1 minute after she hit her head in hockey. According to the Canadian CT head rules, does she require imaging?
Canadian CT head rules are NOT APPLICABLE to patients <16
(or GCS <13, warfarin or bleeding disorder, obvious open skull fracture).
Can use PECARN for pediatric head traumas. According to PECARN, would recommend observation (not CT).
Briefly outline who requires a CT following TBI according to the Canadian CT head rules
Head CT without contrast indicated if GCS 13+ with any of the following:
-LOC
-Anterograde amnesia
-Confusion
-High risk for surgical intervention (age 65+, GCS <15 after 2 hours, vomiting 2+ times, suspected skull fracture)
-Moderate risk for surgical intervention (anterograde amnesia >30 min, dangerous MOI).
Tom comes into the clinic one morning worried he is having a stroke. You do a quick assessment and note complete right sided facial paralysis. What is the most likely lesion?
R ipisilateral facial canal (Bell’s palsy)
Carrie comes into the clinic concerned she is having a stroke. You do a quick assessment and note right sided facial paralysis with sparing of the forehead (i.e., you note forehead wrinkles when you ask her to lift her eyebrows). What is the most likely lesion?
L primary motor cortex (i.e., UMN lesion/ stroke)
Explain why Bell’s palsy paralyses the whole face, but a UMN lesion/ stroke does not
Muscles of the upper face (forehead) are innervated by UMN from both the left and right motor cortex.
Muscles of the lower face receive innervation from UMN ONLY from the contralateral motor cortex.
Pretend you take out the entire L motor cortex…. you have lost all your innervation to the R lower face (recall- gets contralat motor innervation), BUT, the upper face still gets some innervation from the (remaining/ surviving) R motor cortex. So, you can still wrinkle your forehead.
Recall that CN VII (Facial nerve) innervates all the muscles of facial expression. If you cut CNVII, you lose innervation to the ENTIRE side of the face innervated by that nerve. So you can’t wrinkle your forehead.
Isabelle comes in with concerns for a stroke. She can’t move the right side of her face. What findings would help reassure you she is actually suffering from Bell’s palsy?
-Complete R sided facial paralysis, including the forehead
-Onset on waking or over hours (NOT sudden over seconds)
-Denies suffering from the worse headache of her life
-No visual changes, all other CN normal on PE
-No focal neurological deficits
What cranial nerve does Bell’s palsy affect
CN VII facial nerve
Risk factors for Bell’s palsy?
Previous hsv, hzv infection
Recent infection (i.e., URTI)
DM
Pregnancy (esp. 3rd trimester)
Fhx
HTN
Hypothyroid
Describe symptoms of Bells palsy
-Acute onset unilateral facial weakness or paralysis (impaired forehead wrinkling, inability to close eye on affected side, drooping of eyelid, mouth droopin on affected side, flattened nasolabial fold, drooling)
-Decreased tearing
-Hyperacusis
-Pain
-Change in taste
What red flags must you rule out in the evaluation of Bell’s palsy? ?
Forehead sparing (indicates contralateral UMN lesion)
Focal neurological deficits (Bell’s palsy, by nature, only affects one cranial nerve. Presence of focal neuro deficits suggestive of UMN lesion/ stroke)
Bilateral acute facial weakness (i.e., MS),
Fever/ headache/ stiff neck, vesicles in ear canal (Ramsay hunt),
Additional cranial neuropathies,
Sudden onset of symptoms at max severity (Bell’s occurs over 1-3 days and is progressive),
Worsening beyond 3 weeks
Non- pharm tx of Bell’s palsy?
-Facial physical therapy for muscle weakness (following acute stage)
-Eye protection: sunglasses, eye patch, taping eye shut at night (otherwise corneal ulceration and visual impairment can occur)
-Heat/ cold for pain
Pharm tx of Bell’s palsy?
-Medical management is first line
-Focused on reducing inflammation/ nerve compression
-Corticosteroids (ASAP and within 48 hours) (earlier administration leads to improved outcomes/ improved likelihood of full recovery). Corticosteroids are supress inflammation and relieve nerve swelling/ compression. Prednisone (total of 450- 500mg over 10 days; doses should be evenly distributed throughout the day) (Patel et al., 2022; Puckett et al., 2022).
-Antivirals can be combined with steroids (severe cases only; antivirals alone show no clinical benefit). Acyclovir- optimal dosing uncertain, 400mg five times daily or Valacyclovir 1g three times daily
-Acetaminophen for pain
-Eye drops (i.e., methylcellulose) for lubrication
Who/ when to consult/ refer for Bell’s palsy?
Neurology
* Failure to resolve after 4-6 weeks (5-8% of patients reports residual signs/ symptoms)
* Other cranial nerve involvement/ abnormalities
* Recurrence of facial palsy
* Bilateral palsy
Ophthalmology- ongoing ocular pain, corneal ulceration, abraision
Otolaryngologist if surgical decompression considered
When to FU with a patient that you diagnose with Bell’s?
3-4 days, then in 2 weeks
Good red flag teaching
Return if sx worsen
Do you have to send a patient with suspected Bell’s palsy to the hospital to r/o stroke?
No. Bell’s is a clinical diagnosis.
Not recommended to complete imaging (delays time to diagnosis and appropriate treatment with corticosteroids +/- antivirals, unecessary patient anxiety)
Send to ED only if red flags (forehead spared, other CN involved, focal neuro deficits, severe HA, dizziness, etc
What is a primary headache vs secondary headache?
Primary headaches include tension-type headaches, migraines and cluster headaches.
Secondary headaches are caused by an underlying medical disorder/cause ex. drugs, infectious, vascular, neoplastic/tumor, trauma
Which type of primary headache is most prevalent in the adult population?
Tension-type
Gary presents with a history of daily headache attacks over the last few months. They last about 10 minutes, are temporal and described as constant stabbing. The headaches improve where he walks around and seem to be triggered by light. He notes that he often gets a red watery eye on the same side as the pain and nasal congestion with the pain.
Why type of headache is this?
Cluster headaches
Generally there are two types of treatments for headaches. One type is to treat active headaches, and the other is to prevent them. What are the terms for this?
Abortive treatments
Prophylactic treatments
What are the abortive treatments for cluster headaches
Oxygen 100%
Triptans
Ergotamine
What are prophylactic treatments for cluster headaches?
Avoid EtOH
CCB (verapamil)
Anticonvulsants (topiramate)
Lithium
Generally, how frequently do headaches need to occur to be considered chronic?
15 days or more/month for greater than 3 months
What is the pneumonic for diagnosis of migraine? and what does it stand for?
POUND
Pulsatile quality
One-day duration (4-72 hours if untreated/unsuccessfully treated)
Unilateral
Nausea/Vomiting
Disabling intensity
Abortive treatments for migraine
Triptan and/or NSAID +/- antiemetic (metoclopramide)
T/F: Only prescribe anti-emetics for migraine management if the poor soul has severe nausea as a major migraine feature
False - antiemetics can enhance the effects of the other meds and may be helpful even in the absence of nausea
How often did our dear friend Jess need to get migraines before her care provider offered her prophylactic treatment?
According to RxFiles, if greater than or equal to 3-6 headache days/month, offer prophylaxis
There are a bunch of migraine prophylaxis options, including 1st, 2nd and 3rd lines. What are the 4 first line options?
Beta-blocker
Amitriptyline
Topiramate
Candesartan
About half of patients will respond to the top 3 agents with about a 50% decrease in attacks
Red flags symptoms for headache
SNOOP4
- Systemic symptoms of illness: fever, anticoagulation, pregnancy, cancer
- Neurological S/S: impaired mental status, neck stiffness (meningismus), seizures, focal neurological defects
- Onset: sudden and severe, new headache after age 50
- Other associated conditions: following head trauma, awakens from sleep, jaw claudication, scalp tenderness
- Pattern change, positional, progressive, precipitated by Valsalva
This type of headache occurs without nausea and with 2 or more of the following:
Bilateral
Non-pulsating
mild-moderate pain
not worsened by activity
Tension Type Headaches
Abortive treatments for TTH
Ibuprofen, ASA, naproxen, acetaminophen
Prophylactic treatment for TTH
1st line: amitriptyline, nortriptyline
2nd line: mirtazapine, venlafaxine
But wait! what about lifestyle management? Can’t peeps try anything to help themselves aside from taking the drugs?
Yes!
Headache diary to identify triggers
Adjust lifestyle: reduce caffeine, exercise regularly, optimize sleep and nutrition/regular meals
Manage stress: relaxation training, CBT, pacing activity, biofeedback
What about medication overuse headaches? What types of medications are those talking about?
Ergots, triptans, combination analgesics or codeine/other opioids ≥ 10 days a month OR
Acetaminophen or NSAIDs ≥ 15 days a month
The illusion of self or environmental movement, typically rotating, spinning, tilting, or a sensation one is going to fall down
Vertigo
Vertigo can be central or peripheral. Which is more common?
Central vertigo - 15%
Peripheral - 85%
Central vertigo comes from the brainstem or cerebellum - what are some examples of etiologies?
Tumor
Stroke
Drugs
MS
Peripheral vertigo comes from the inner ear or vestibular nerve - what are some examples of etiologies?
Idiopathic
Meniere’s
BPPV
Acoustic neuroma
Trauma
Drugs
Labyrinthitis
What key difference can be used to differentiate central and peripheral vertigo?
Central presents with other /persistent neuro abnormalities
Ex. double vision, dysarthria, dysphagia, paresthesia, motor/sensory changes
What is the most common etiology of peripheral vertigo?
BPPV (50%)
BPPV is caused by migration of otoliths within the inner ear resulting in slightly difference signals being perceived by the brain and the two sensation organs, giving the perception of movement.
What are some predisposing factors to this?
Head injury
URTI
Degenerative disease
Idiopathic
How do you diagnose BPPV?
Dix-Hallpike maneuver
Patient sits with head turned 45 degrees and eyes open
Help patient to lean back with one ear pointed to the ground over the edge of the table - stay there 1-2 minutes
Nystagmus is positive for BPPV
The patho of Restless Leg Syndrome (RLS) is not completely understood.
What are some of the most commonly identified central nervous system correlates in patients with this condition?
Reduced CNS iron stores.
Unclear correlation b/n dopaminergic systems and RLS
A variety of other neurotransmitter abnormalities may be at play - preliminary data re: endogenous opioids, glutamate and glutamine, adenosine, histamine, GABA.
Thalamic correlates - thalamic abnormalities often reported in patients with RLS.
Network connectivity - most commonly impacting the thalamus and pons.
Identified risk factors for Restless Leg Syndrome?
Family hx
Low iron stores
Uremia secondary to renal failure is strongly assoc. w/ s/s of RLS.
Neuropathy
Spinal cord disease
Pregnancy
MS
Parkinsons
Possible link b/n essential tremor and RLS
Antihistamines, dopamine receptor antagonists, and certain antidepressants such as mirtazapine, TCAs, SSRIs and SNRIs may exacerbate this condition:
Restless Leg Syndrome
DDX of Restless Leg Syndrome
Volitional movements
Akathisia
Nocturnal leg cramps
Positional discomfort
Leg pain
Physiologic leg movements during sleep
Here are the 5 diagnostic criteria for Restless Leg Syndrome. All 5 need to be present for a diagnosis.
●An urge to move the legs, usually accompanied or caused by uncomfortable and unpleasant sensations in the legs. Sometimes the urge to move is present without the uncomfortable sensations, and sometimes the arms or other body parts are involved in addition to the legs.
●The urge to move or unpleasant sensations begin or worsen during periods of rest or inactivity such as lying or sitting.
●The urge to move or unpleasant sensations are partially or totally relieved by movement, such as walking or stretching, at least as long as the activity continues.
●The urge to move or unpleasant sensations are worse in the evening or night than during the day, or only occur in the evening or night. When symptoms are severe, the worsening at night may not be noticeable but must have been previously present.
●Symptoms are not solely accounted for by another medical or behavioral condition, such as leg cramps or habitual foot tapping.
Treatment recommendations for RLS?
Iron - oral or IV
behavioural strategies
Avoidance of aggravating factors
Ensure sufficient sleep
Review med S/E for possible contributors
Carbidopa-levodopa for intermittent symptoms
Clonazepam for intermittent episodes in younger people
Gabapentinoids for chronic RLS.
Dopamine agonists in small doses for chronic RLS
If unresponsive to above, may consider low-potency opioid therapy such as codeine or tramadol, or high-potency such as morphine, oxycodone, hydrocodone, methadone.
What is trigeminal neuralgia? (TN)
Trigeminal neuralgia (TN) is characterized by recurrent brief episodes of unilateral electric shock-like pains, abrupt in onset and termination, in the distribution of one or more divisions of the fifth cranial (trigeminal) nerve that typically are triggered by innocuous stimuli.
The trigeminal nerve is the sensory supply to the face and the sensory and motor supply to the muscles of mastication. It has three major divisions:
●Ophthalmic (V1)
●Maxillary (V2)
●Mandibular (V3)
What are polyneuropathies?
Chronic progressive involvement of multiple peripheral nerves in symmetrical, distal-predominant pattern
*there are a variety of types of peripheral neuropathies but we will focus on this kind…
TN is a rare condition that affects F>M, with annual incidence of 3-4 per 100,000. Despite this, it is one of the more frequently seen neuralgias in which population?
Older folks.
The incidence increases gradually with age; most idiopathic and classic TN cases begin after age 50, although onset may occur in the second and third decades or, rarely, in children.
What is the most common kind of polyneuropathy?
Other common causes?
Diabetes Mellitus polyneuropathy
Other common ones are from alcohol abuse and HIV
Patho of peripheral neuropathies?
Peripheral nerves are susceptible to a variety of toxic, inflammatory, hereditary, infectious and parainfectious factors that can impair health and function and lead to the clinical disorder of polyneuropathy.
Often relates to complex inflammatory, metabolic and ischemic effects
Mechanisms include ischemic, axonal, infiltrative and demyelination
What medications can cause peripheral neuropathy?
chemotherapeutic drugs, antimicrobials (dapsone, fluoroquinolones, isoniazid, metronidazole, nitrofurantoin), amiodarone, colchicine, disulfiram, phenytoin
What environmental factors cause peripheral neuropathy?
vibration-induced nerve damage, prolonged cold exposure, hypoxemia
What is an example of an acute cause of peripheral neuropathy
Guillain-Barré syndrome (GBS)
Examples of
1) subacute
2) chronic
causes of peripheral neuropathy
sub-acute =medication induced
chronic = DM
General presentation of peripheral neuropathy?
Symmetric distal sensory loss, burning sensations or weakness
Can be mild/asymptomatic and only identified on detailed sensory examination of lower extremities
Now we are going to talk about some different kinds of neuropathies…
In Chronic axonal neuropathies:
1) Injury is related to axon length so ____ axons are affected first
2) Are sensory or motor symptoms seen first?
Longer
Sensory symptoms precede motor symptoms. Distal loss of sensation to pinprick, light touch, vibration, cold and proprioception
Also regarding chronic axonal neuropathies:
1) how are reflexes affected if at all?
2) Is gait affected? What about strength?
3) Slow or fast progression?
4) What can happen in severe cases?
Hypoactive to absent distal reflexes
Slowly progressive sensory loss, numbness/burning/pain in feet, mild gait abnormalities
As it progresses, leads to mild weakness in lower legs and hand symptoms “Stocking and glove” distribution
In severe cases numbness can extend and effect intercostal nerves (sensory loss over sternum and eventually the top of head)
Describe acute axonal neuropathies
Similar but more severe and sudden symptoms – pain often predominant
Worsens over 2-3 weeks, plateaus, and recovers over months
Usually dose related, but can occur within days of drug exposure
What occurs in demyelinating neuropathy?
Typically effects motor system more so than sensory
Generalized weakness, reduced sensation, diffusely reduced or absent reflexes
Key aspects of history taking for someone with peripheral neuropathy?
HPI
Recent viral illnesses, other systemic symptoms, new medications, exposures to solvents/heavy metals/toxins, alcohol use, family history of neurological disease
Key differential causes for symmetric polyneuropathies?
Vascular: SLE, RA, PAN
Infectious: HIV, leprocy, lyme
Immune: GBS, CIOP
Hereditary
Neoplastic
Toxin (Etoh, heavy metals, meds)
Metabolic: DM, hypothyroidism, renal failure
Nutritional: B12 deficiency
Other: porphyria, amyloid
Highest yield tests for determining etiology in symmetric polyneuropathy:
lood glucose, B12 levels with methylmalonic acid and serum protein electrophoresis (SPEP)
Additional diagnostics we may need to use:
Perform electrodiagnostic testing: electromyography (EMG) or nerve conduction studies (NCS) - this will determine if neuropathy or myopathy and whether axonal or demyelinating
Additional possible tests: LP, genetic testing, muscle or nerve biopsy
Etc
T/F Hypothyroid polyneuropathy improves with thyroid replacement
True!
T/F Diabetic neuropathy is reversible with tight glucose control
No
But tight glucose control may help maintain nerve function
T/F Treatment of rheumatic diseases halts progression of neuropathies
True!
How do we treat the symptoms of neuropathies?
Gabapentin and TCAs can be used to reduce pain
Other options: duloxetine, pregabalin, carbamazepine, phenytoin, topiramate, baclofen, mexiletine and dextromorphan
Additional treatment with NSAIDs or low-dose narcotics may be needed for breakthrough pain
PT – splints, walking assistive devices
There is Increased risk for gait instability and falls due to progressive loss of proprioception and foot pain… what can we do about this to prevent these issues in our patients?
PT/OT/home evaluation
For diabetics: how often should we be inspecting their feet and how often should be do comprehensive foot exams (including sensation testing, etc)
Visually inspect feet at each routine visit
Perform comprehensive foot exam annually
Definition and etiology of GUillain-Barre Syndrome?
(not sure if Sarah wants us to know about GBS but it’s a form of peripheral neuropathy so I’m throwing it in here…)
Definition
* acute (evolving over 4 wk or less) rapidly evolving demyelinating infammatory
polyradiculoneuropathy that ofen starts in the distal lower limbs and ascends
Etiology
* autoimmune attack and damage to peripheral nerve myelin
* sometimes preceded by viral/bacterial infections
S&S of GBS
- where does it start?
- asymmetric or symmetric?
- motor, sensory, or both?
- autonomic effects?
- sensory: distal and symmetric paresthesias, loss of proprioception and vibration sense, neuropathic
pain - motor: weakness starting distally in legs and progressing proximally, arefexia
- autonomic: blood pressure dysregulation, arrhythmias, bladder dysfunction
Treatment of GBS
IVIG or plasmapheresis, pain management, monitor vitals and vital capacity
When do the symptoms of GBS usually peak and then resolve?
Mortality rate?
peak of symptoms at 2-3 wk, plateau or resolution at 4-6 wk
- 5% mortality (higher if require ICU), up to 15% have permanent defcits
What are some clinical features of trigeminal neuralgia?
●Trigeminal distribution – The pain of TN is strictly limited to the distribution of the trigeminal nerve.
●Paroxysmal pain - The pain of TN tends to occur in paroxysms and is maximal at or near onset. Facial muscle spasms can be seen with severe pain, often described as electric, shock-like, or stabbing. It usually lasts from one to several seconds, but may occur repetitively, anywhere from 0 to more than 50 times a day. TN typically does not awaken patients at night.
●Unilateral – TN is typically unilateral. Occasionally the pain is bilateral over time, though rarely on both sides simultaneously.
●Trigger zones – Nearly all patients with TN experience triggered pain. Trigger zones in the distribution of the affected nerve are common and are often located near the midline. Lightly touching these zones often triggers an attack, leading patients to protect these areas. Other triggers of TN paroxysms include chewing, talking, brushing teeth, cold air, smiling, and/or grimacing.
●Autonomic symptoms – Autonomic symptoms, usually mild or moderate, can occur in association with attacks of TN in the V1 trigeminal distribution, including lacrimation, conjunctival injection, and rhinorrhea.
●Continuous pain – Continuous pain between attacks is present in many patients with TN. It is usually milder than the paroxysmal attacks and is typically characterized as dull or tingling, though the intensity and quality may fluctuate.
The International Classification of Headache Disorders, Third Edition (ICHD-3) diagnostic criteria for TN are as follows:
●A) Recurrent paroxysms of unilateral facial pain in the distribution(s) of one or more divisions of the trigeminal nerve, with no radiation beyond, and fulfilling criteria B and C.
●B) Pain has all of the following characteristics:
*Lasting from a fraction of a second to two minutes
*Severe intensity
*Electric shock-like, shooting, stabbing, or sharp in quality
●C) Precipitated by innocuous stimuli within the affected trigeminal distribution
●D) Not better accounted for by another ICHD-3 diagnosis
Etiology of essential tremor?
Largely unknown
Strong genetic component - first degree relatives at inc risk of developing it, especially if onset before 40
What do we know about the patho of essential tremors?
Genetic heterogeneity suggest may be syndrome of related disorders, not single disease
Neuropathologic basis of ET poorly defined but thought to involve cerebellum and brainstem
What body parts does essential tremor (ET) commonly affect?
Classically affects hands and arms
Can also affect head, voice,
less commonly face or trunk
Is ET typically unilateral or bilateral?
Bilateral
Often slightly asymmetric
Is ET have a slow or fast progression?
What worsens the progression?
Slowly progressive
worsened by anxiety, medical illness or new medications
ET is an action tremor. What does this mean?
What positions will make the tremor show up?
Tremor is brought out by arm movement and when arms held in fixed posture against gravity – will see is very apparent when arms are outstretched
Amplified by goal directed movements such as drinking from glass or finger-to-nose testing
T/F ET is seen when hands are at rest
False
Tremor absent when the affected body part is fully relaxed and supported against gravity
What kind of daily activities are commonly affected by ET?
Affects common daily activities such as writing, drinking from a glass, and handling eating utensils
T/F ET is usually a low frequency tremor
False(ish)
Tremor typically moderate to high frequency but lots of variation
If essential tremor is seen in the head, what will it look like?
Tremor in head can be vertical (“yes-yes”) or horizontal (“no-no”) - will see associated hand or voice tremor
T/F One diagnostic tool for ET is to see if the tremor lessens when the patient drinks a small glass of wine.
True!
T/F ET is worsened by caffeine intake
False!
In contrast to a physiologic tremor, ET is NOT usually exacerbated by caffeine
What makes the tremor of ET worse?
anxiety, excitements, or other adrenergic stimulation
T/F Lower limb tremors are common in ET
False
Lower limb tremor highly unusual for ET and usually suggests Parkinsons
Do we typically see additional neurologic manifestations beyond the tremor in ET?
By definition, should be the ONLY neurologic manifestation. However, difficulty with tandem gait, mild cognitive impairment, and slight overflow of the tremor into a resting posture may be present (aka “soft neurologic signs” or “ET Plus”)
DDx for ET
Parkinsonism tremor
Enhanced physiologic tremor
Dystonic head tremor
And others
What are the symptoms of parkinsons? How are they different from ET?
Most common cause of resting tremor
Onset usually unilateral
Abnormal findings on neuro exam: bradykinesia, limb cogwheel rigidity
Tremor more likely in jaw or lips (in ET, more common in head or neck)
Can have overlap: not uncommon to see PD patients to present with postural tremor before other S&S
- A rest tremor involving the foot or legs almost always suggests a parkinsonian tremor
What distinguished ET from a physiologic tremor?
Physiologic tremor resolves when you remove the precipitating factor
(such as stress, anxiety, excitement, muscle fatigue, fever, hypoglycemia, alcohol or opioid withdrawal, and a variety of medications, drugs, and substances)
Brief description of the tremor seen in essential tremor:
1) Symmetric or asymmetric?
2) High or low frequency? Amplitude?
symmetrical, very low-amplitude, high-frequency physiologic action tremor in the upper limbs
What are some key diagnostics to complete to differentiate ET and essential tremor?
- Review medication list
- Check TSH, lytes including Calcium
(there’s a great algorithm in Up to Date)
What imaging should you order if you suspect/diagnose trigeminal neuralgia?
MRI with and without contrast to rule out neurovascular compression or a structural brain lesion. CT is an alternative when MRI is not an option, but MRI and magnetic resonance angiography (MRA) are much preferred because the higher resolution of MRI enables visualization of the trigeminal nerve and small adjacent lesions.
T/F If you suspect essential tremor, get an MRI.
False
MRI or CT is NOT indicated in those with typical clinical features of ET
DDX for trigeminal neuralgia?
acute herpes zoster
postherpetic neuralgia
trauma to the trigeminal nerve
dental pain
causes of headache
What are the diagnostic criteria for ET?
Diagnostic criteria:
Core criteria:
- isolated tremor syndrome consisting of bilateral upper limb action tremor
- Absence of other neuro symptoms
- with or without head, voice, and/or lower limb tremor
Secondary criteria:
- >3 years in duration
- Positive family hx
- Beneficial response to alcohol
What is the 1st line tx for trigeminal neuralgia?
As per UTD:
For patients with TN who require pain control, we recommend initial therapy with carbamazepine or oxcarbazepine.
Carbamazepine — Carbamazepine is the best studied treatment for classic TN and is established as effective. Side effects can be a problem but are generally manageable, particularly if low doses are prescribed initially with gradual titration.
Oxcarbazepine is an effective drug for TN and one that some experts prefer over carbamazepine, citing better tolerability and decreased risk of drug interactions.
If these are CI, can consider treatment with lamotrigine, gabapentin, or baclofen.
There are a few surgical options but those conversations happen with someone we refer to.
Name the exclusion criteria for essential tremor
- Isolated focal tremors (voice, head)
- orthostatic tremor
- Task or position-specific tremors
- Sudden onset and stepwise deterioration
Treatment of ET
What 2 meds do we use?
How do we use them?
Symptomatic only
If possible, d/c any medications or substances that worsen tremor
½ glass of wine or other small amount alcohol in social situations can be used to decrease symptoms
Offer pharmacotherapy if intermittent or persistent disability caused by tremor
If frequent/daily symptoms: daily propranolol or primidone (Equal efficacy)
If situational exacerbations: (such as social occasions or public performances) can use Intermittent drug treatment (usually propanolol)
T/F the goal of treatment for ET is complete remission
Usually goal is to decrease tremor severity to prevent disability
If tremor minor: may be able to get complete remission with medication.
Important to tell patient that tremor will worsen with time, may need to add secondary agent
Prognosis for ET?
Slow, gradual progression of tremor, which usually occurs over years
Earlier onset correlates with slower progression
Is disabling condition for majority of patients
How is BPPV treated?
Epley maneuver - immediate resolution in 85-95%
OR
Brandt-Daroff exercises (patient can do on their own)
Anti-emetics
Describe the Epley maneuver. Why does it work?
The Epley maneuver is a canalith repositioning procedure - it works by removing crystals trapped in the semicircular canal
Turn head to affected side 45 degrees
Keeping head turned, lay patient back with head extended 10-20 degrees off the edge of the table
Turn head toward unaffected side
Turn head another 90 degrees by rolling body to unaffected side
Sit patient up while keeping head turned and neck flexed
Meniere’s disease presents with a triad of which symptoms?
Vertigo, tinnitus, hearing loss
Other presenting symptoms include: aural fullness, N/V, drop attacks
What is the patho of Meniere’s?
Inadequate absorption of endolymph hydrops (over accumulation) that distorts the membranous labyrinth
What are triggers for Meniere’s attacks?
High salt diet, caffeine, stress, nicotine, alcohol
T/F: Hearing loss from Meniere’s disease is permanent
True :(
Mrs. Claus presents with tinnitus, episodic dizziness and ear pain. After conducting her history, you think this sounds like Meniere’s. Would you order any diagnostics to establish this diagnosis?
Audiometric confirmation of low-mid frequency SNHL required for diagnosis
Additional diagnostic criteria: 2 or more spontaneous episodes of vertigo lasting 20 mins -12 hours and fluctuating tinnitus and/or aural fullness.
In summary, what are the differentiating features on the history/physical between BPPV and Meniere’s?
BPPV is usually initiated by certain head movements - Meniere’s is not.
BPPV vertigo spells are brief, Meniere’s vertigo spells last minutes-hours.
On the physical exam, the hearing screens will likely be abnormal for Meniere’s
Meniere’s will present with additional symptoms of aural fullness, tinnitus and hearing loss.
