TEST 4-STUDY GUIDE-2 Flashcards by Rachel Welsh

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Exacerbating factors: fatigue, lack of sleep, poor posture, anxiety, stress, depression

tension headaches

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What are the clinical features of tension headaches?

Episodic nature
Headaches last 30 minutes to a couple of days.
Holocranial or bifrontal, band-like headache (mild to moderate intensity)
Dull, pressing, nonpulsating (“vice-like”) quality
Headache does not increase with exertion.
Maximum of one autonomic symptom (phonophobia or photophobia)
No nausea, vomiting, or aura
Palpation of muscles of the head may reveal increased pericranial tenderness

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What is the diagnostic criteria for tension headache?

At least two of the following:
Dull, pressing, nonpulsating quality
Mild to moderate intensity
Bilateral
No increase in intensity with exertion

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Both pharmacologic and nonpharmacologic strategies can be used for the treatment of tension-type headache. In addition, any underlying conditions (e.g., depression) should be identified and treated.

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Episodic tension-type headache treatments?

NSAIDs (e.g., ibuprofen, aspirin) or acetaminophen

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Chronic/frequent tension headache?

frequent episodic type: consider prophylactic therapy (e.g., with amitriptyline).

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DO NOT GIVE TRIPTANS IN FOR THE TREATMENT OF TENSION TYPE HEADACHE!!
AVOID OPIODES

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Non pharm treatment?

lifestyle, weight reduction
CBT

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Counsel patient against taking acute pain medication for more than 15 days/month to avoid medication overuse headache.

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Treatment for episodic tension headache?

One of the following NSAIDs:
Ibuprofen
Naproxen
Diclofenac
Aspirin
Ketorolac IM
Acetaminophen
Caffeine DOSAGE can be used in combination with ibuprofen or acetaminophen to augment the analgetic effect.

Counsel patient against taking acute pain medication for more than 15 days/month to avoid medication overuse headache.

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What is prophylactic therapy for tension type headaches?

Prophylactic therapy for chronic tension-type headache and frequent episodic tension-type headache [5][6]
First-line: amitriptyline (TCA) -black box suicide warning risk - migraine prophylaxis, tension headache prophylaxis, depression, neuropathic pain, can use breastfeeding low risk fetal harm

no not give prolonged QT, closed angle glaucoma, alcohol abuse

Second-line
Mirtazapine (TCA)
Venlafaxine (SNRI)- MDD, GAD, social anxiety, panic disorder

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What is some non-harm treatment for tension headaches?

Lifestyle and behavioral changes (identification and management of triggers)
Reduction of caffeine intake
Smoking cessation
Stress reduction
Sleep hygiene
Physical activity
Treatment of underlying conditions (e.g., depression)
Additional nonpharmacological therapies include: [5]
Biofeedback
Relaxation training (e.g., progressive muscle relaxation)
Cognitive behavioral therapy
Physical therapy (including posture training, massage, spinal manipulation)
Acupuncture

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What is the acute management for tension type headache?

Rule out red flags for headache and check for signs of high-risk headache.

Pharmacotherapy with NSAIDs, aspirin, or acetaminophen (see “Treatment” above)

Counsel patient against taking NSAIDs for more than 15 days per month.

Recommend lifestyle and behavioral changes.

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The most appropriate preventive medication for chronic tension-type headache is amitriptyline.

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Classic tension-type headaches are bilateral and of mild to moderate intensity, with a pressing or tightening (nonpulsating) quality. They do not worsen with activity and are not associated with nausea or vomiting. They can be associated with photophobia or phonophobia but not both. The key physical finding is pericranial muscle tenderness, which can be assessed by palpating the pericranial muscles (frontalis, temporalis, masseter, pterygoid, sternocleidomastoid, splenius, and trapezius).

Treatment for acute tension-type headache includes aspirin or nonsteroidal antiinflammatory drugs. Preventive treatment can be considered for patients who do not respond to acute treatment and for those with frequent headache (1 to 14 headache days per month) or chronic headache (≥15 headache days per month).

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cluster headaches

While patients with migraine headaches tend to rest motionlessly in a quiet, dark room, individuals with cluster headache pace around restlessly in excruciating pain!

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Sex: ♂ > ♀ (3:1) [1]
Peak incidence: 20–40 years [2]
Prevalence: rare, ∼ 0.1% of general population [1]
Epidemiological data refers to the US, unless otherwise specified.

cluster headache

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The etiology of cluster headache is not entirely understood but is thought to involve a genetic component/ Risk factors

tobacco use
Triggers of cluster headache
Alcohol
Histamine
Seasonal fluctuations
Nitroglycerine
Volatile substances (solvents, oil-based paint)

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What are the characteristics of a tension headache?

Agonizing pain!!

Strictly unilateral, periorbital, and/or temporal
Quickly developing (within minutes), short, recurring attacks that usually occur in a cyclical pattern (“cluster periods”)
May become chronic (less common), with interruptions of less than three months between cluster bouts [
Attacks often wake patients up during sleep.

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What are the ipsilateral autonomic symptoms for cluster headaches?

Ipsilateral autonomic symptoms

Conjunctival injections and/or lacrimation
Rhinorrhea and nasal congestion
Partial Horner syndrome: ptosis and miosis, but no anhidrosis
Restlessness and agitation

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What is the treatment for cluster headaches? 1st line therapy?

Oxygen therapy with FiO2 100%: usually the first choice if available

Triptans
Subcutaneous sumatriptan
Or intranasal zolmitriptan

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True or False for treatment of cluster headaches?

Standard analgesics (e.g., acetaminophen, NSAIDs, opioids) are not recommended because they are ineffective and may lead to medication overuse headache if used frequently. [19]

To improve absorption, apply nasal sprays in the nostril unaffected by congestion.

For treatment of cluster headache

What is prophylactic treatment for cluster headaches?

verapamil- calcium channel blocker

The most effective acute abortive treatment for cluster headache is 100% oxygen or sumatriptan.

This patient's presentation is most consistent with cluster headache. Most patients with cluster headaches experience 1 to 2 headache attacks daily, but the pattern can vary from every other day to 8 times per day. The attacks can last from 15 minutes to 3 hours and tend to recur at the same time of day. Cluster headaches are often episodic, with remission and recurrence sometimes timed with the seasons. The most effective acute abortive treatment options for cluster headaches include sumatriptan (by injection or nasal administration) or 100% high-flow oxygen (administered at 10 to 15 liters per minute for 15 to 30 minutes). Verapamil is the drug of choice for preventive therapy.

This patient's history is consistent with cluster headache. Cluster headache is diagnosed clinically based on the occurrence of at least five attacks that (a) last 15 to 180 minutes each; (b) are characterized by severe unilateral pain in the orbital, supraorbital, and/or temporal region; (c) are accompanied by at least one autonomic sign or symptom ipsilateral to the headache, a sense of restlessness or agitation, or both . To meet diagnostic criteria, the attacks must occur at least once every other day and up to 8 times daily for more than half the time that the disorder is active.

The occurrence of five or more attacks of a severe unilateral orbital headache with associated prominent autonomic symptoms but no prodrome or photophobia is most consistent with cluster headache.

____ are primarily muscular, manifesting with a classic band of pain around the head. The symptoms can be reproduced with palpation, are often bilateral, and are not associated with autonomic symptoms.

tension type headache

____ manifest similarly to cluster headaches, but the lack of prodrome or photophobia in this patient’s history makes migraine a less likely diagnosis in this case.

migraine

cluster headaches occur on a seasonal basis

__ falls under the category of trigeminal autonomic cephalagias? TACs

primary headache disorder- severe unilateral head pain with ipsilateral autonomic symptoms 1 of the most painful types of headaches Occur more in men cluster= more like clockwork!!

Name: Linda T. - Age: 30 - Occupation: Administrative Assistant **Clinical Presentation:** Linda comes to the clinic with a 4-month history of headaches that occur twice a week. She describes the pain as a dull, pressing tightness around her head, which she likens to a tight band. The headaches are mild to moderate in intensity, bilateral, and do not worsen with physical activity. She denies any nausea or vomiting, but occasionally feels slightly more sensitive to noise. **Question 1:** Based on Linda's symptoms, which characteristic supports the diagnosis of a tension-type headache? A) Pulsating, moderate to severe headache - B) Bilateral dull, pressing head pain - C) Increased pain with exertion - D) Accompanied by nausea and photophobia

Answer:** B) Bilateral dull, pressing head pain **Rationale:** Tension-type headaches are typically described as bilateral with a dull, pressing, non-pulsating quality. They differ from migraines, which can be unilateral, pulsating, or associated with nausea and photophobia.

What would be an appropriate first step in managing Linda’s tension-type headaches? - A) Prescribe a triptan for acute relief - B) Recommend NSAIDs as needed and incorporate stress-reduction techniques - C) Start a daily prophylactic medication like a tricyclic antidepressant - D) Perform imaging studies to rule out secondary causes

Answer:** B) Recommend NSAIDs as needed and incorporate stress-reduction techniques **Rationale:** Initial treatment for tension-type headaches often involves simple analgesics like NSAIDs (e.g., ibuprofen or acetaminophen) and non-pharmacologic approaches such as stress management. Prophylactic medications or imaging studies are not usually warranted unless headaches do not respond to initial treatments or present with atypical features.

**Patient Profile:** - Name: John D. - Age: 45 - Occupation: High School Teacher **Clinical Presentation:** John has been experiencing daily headaches for 5 months. He describes them as continuous and feels like head pressure that fluctuates in intensity. The pain is non-throbbing and bilateral. He notices no associated symptoms like nausea or visual disturbances. He sometimes works long hours and has a high-stress work environment. **Question 1:** For John, who has chronic tension-type headaches, what non-pharmacologic interventions could be emphasized as part of his treatment plan? - A) Regular aerobic exercise and relaxation techniques - B) High-dose vitamin supplements - C) Restrictive water intake to reduce cerebrospinal fluid pressure - D) Sugary diet changes to combat fatigue

Answer:** A) Regular aerobic exercise and relaxation techniques **Rationale:** Non-pharmacologic interventions such as regular physical activity and relaxation strategies can help manage chronic tension-type headaches. These lifestyle changes address stress and tension, common contributors to this headache type. Excessive vitamin supplementation, restricted hydration, or sugary diet changes are not standard recommendations.

*Question 2:** If John's headaches do not improve with lifestyle modifications and NSAIDs, what could be a next step in pharmacologic management? - A) Initiate a trial of a tricyclic antidepressant like amitriptyline - B) Prescribe narcotics for pain control - C) Treat with beta-blockers as a preventative measure - D) Use triptans routinely

* A) Initiate a trial of a tricyclic antidepressant like amitriptyline **Rationale:** For chronic tension-type headaches unresponsive to NSAIDs and lifestyle changes, a tricyclic antidepressant such as amitriptyline can be effective as a prophylactic treatment. Opioids and triptans are generally not appropriate for treating tension-type headaches. Beta-blockers are more commonly used for migraine prevention.

cluster headache these do not pulsate or cause nausea

BUT migraines cause pulsating and nausea, made worse with activity

If a 60 year old patient comes in with a headache that is the worst of his life

look for tempural arteritis or intracranial hemorrhage

Worst headache of their life - max intensity under 1 minute.

subarachnoid hemorrhage ruptured intracranial aneurysm This needs emergency eval!!!

Thunderclap headache- subarachnoid hemorrhage

rupture of an aneurysm involving the circle of Willis (aneurysmal SAH). Nontraumatic SAH typically manifests with sudden and severe headache, which may be accompanied by nausea, vomiting, signs of meningism, and/or acute loss of consciousness. The best initial diagnostic test is a head CT without contrast, in which acute subarachnoid bleeding can be seen as hyperdensities in the subarachnoid space. If a head CT is negative for SAH, this diagnosis can be ruled out in many patients. However, if clinical suspicion remains high, it may be necessary to perform a lumbar puncture or CT angiography. Once SAH is confirmed, angiography is always necessary in order to identify the source of bleeding (e.g., aneurysms or other vascular abnormalities) and plan definitive treatment. The management of traumatic and nontraumatic SAH consists mostly of neuroprotective measures (e.g., control of blood pressure) to prevent secondary brain injuries. In aneurysmal SAH, microsurgical clipping or endovascular coiling of the aneurysm is indicated to prevent potentially fatal rebleeding. Aneurysmal SAH has a high mortality rate as a result of complications such as rebleeding and delayed cerebral ischemia.

head trauma= cause of SAH

traumatic

non traumatic SAH

ruptured cerebral aneurysm

Thunderclap headache?

Sudden, severely painful headache (often described by patients as the worst headache they have ever experienced)

kernig sign

A physical finding elicited by placing the patient in supine position, flexing the thigh at the hip, and subsequently extending the knee. Considered positive if extension of the knee causes pain and resistance. Suggests meningeal or nerve root irritation.

brudzinski sign

A physical finding in which forced flexion of the neck elicits an involuntary flexion of the knees and hips. It can occur in patients with meningeal irritation secondary to meningitis or subarachnoid hemorrhage.

Best diagnostic test for thunderclap headache?

CT without contrast

Oral nimodipine should be given after SAH to reduce the risk of ischemia associated with vasospasm. This patient's sudden-onset neurologic deficit five days after SAH is a common manifestation of vasospasm, which occurs as a complication of ∼ 30% of SAH cases and is more common with aneurysms. This patient should be evaluated with CT scan and angiography to distinguish potential vasospasm from rebleeding and receive prompt treatment to prevent ischemic stroke.

noncontrast CT scan of the head is the best initial test to assess for subarachnoid hemorrhage, as it is readily available in most hospitals, highly sensitive, and may be performed rapidly. SAH requires rapid diagnosis and treatment because it can quickly cause death if bleeding persists. Any patient who presents with a sudden, severe headache must have SAH ruled out with a head CT scan. If the head CT scan is negative for SAH, but clinical suspicion remains high, a lumbar puncture is indicated. A negative head CT scan and negative lumbar puncture rule out acute SAH. Analgesia, IV fluids, and seizure prophylaxis are initiated if SAH is diagnosed. Further treatment depends on the suspected cause of the hemorrhage. In this patient's case (suspected ruptured aneurysm), surgical clipping would likely be attempted.

Ruptured saccular aneurysms are the cause of 80% of nontraumatic subarachnoid hemorrhages. This patient has several risk factors for the development of a saccular aneurysm, including age > 40 years, female gender, hypertension, and cigarette smoking. Other risk factors for a saccular aneurysm include heavy alcohol use, connective tissue disorders, polycystic kidney disease, and family history.

Sudden-onset headache, nuchal rigidity, and diffuse hemorrhage at the base of the brain on a CT scan are suggestive of a subarachnoid hemorrhage.

Oral nimodipine should be given after subarachnoid hemorrhage to prevent vasospasm, which can lead to ischemic stroke. This patient's sudden-onset neurologic deficit 7 days after SAH is a common presentation of vasospasm, which is a complication in ∼ 30% of SAH cases and is more common with aneurysms. Nimodipine has been shown to reduce morbidity and mortality associated with SAH, but the exact mechanism of benefit of nimodipine is unknown. This patient should be evaluated with CT and angiography in order to distinguish a potential vasospasm from rebleeding and should receive prompt treatment to prevent ischemic stroke.

This patient has a typical presentation of a subarachnoid hemorrhage. By far, the most common cause of nontraumatic subarachnoid hemorrhages is a ruptured intracranial aneurysm. Intracranial aneurysms are abnormal focal outpouchings of cerebral arteries that can occur in any part of the intracranial circulation.

: Ruptured intracranial aneurysms are the most common cause of nontraumatic subarachnoid hemorrhages.

A noncontrast CT scan of the head is the best initial test to assess for subarachnoid hemorrhage, as it is readily available in most hospitals, highly sensitive, and may be performed rapidly. SAH requires rapid diagnosis and treatment because it can quickly cause death if bleeding persists. Any patient who presents with a sudden, severe headache must have SAH ruled out with a head CT scan. If the head CT scan is negative for SAH, but clinical suspicion remains high, a lumbar puncture is indicated. A negative head CT scan and negative lumbar puncture rule out acute SAH. Analgesia, IV fluids, and seizure prophylaxis are initiated if SAH is diagnosed. Further treatment depends on the suspected cause of the hemorrhage. In this patient's case (suspected ruptured aneurysm), surgical clipping would likely be attempted.

A sudden onset severe headache, often described as a 'thunderclap headache' or 'worst headache of my life,' is highly suggestive of

a subarachnoid hemorrhage.

What is dizzinesss versus vertigo?

dizziness- sensation of unsteadiness or off-balance, light headedness, spinning.movement

What is the definition of dizziness?

Sensation of unsteadiness or feeling off-balance, light-headedness or spininning/movement

Vertigo def?

False sensation of rotation or movement of the patient or the patients surroundings

What does vertigo result from?

inner ear disease or the disturbance of the vestibular center or pathways in the CNS

What are the underlying etiologies of dizziness?

-orthostatic hypotension -med side effects -balance disorders If severe orthostatic hypotension can cause LOC, feeling of faintness after laying down may occur which may cause dizziness to occur.

True or false both dizziness and vertigo may cause unsteady gait?

True

What happens with vertigo?

Nausea, vomitting, nystagmus

Look into other neuro sx's with dizziness and vertigo

ataxia cranial nerve dysfunction numbness weakness CNS affecting the cerebellum or brainstem

dizziness/Lightheadedness-> orthostatic hypotension, cardiac arrthmia, vasovagal- cardio workup, orthostatic vitals, basic labs, glucose, HGB

Vertigo (sensation of movement) 1. Dix-Hallpike manuever if episodic vertigo to confirm Benign Parozysmal Positional Vertigo- treat with Epley maneuver vestibular PT 2. HINTS exam? - If persistent vertigo to differeniate peripheral vestibular neuritis or labrynths from stroke treat supportive care antiemetics, meclizine 3. Rule out central vertigo (brainsteam or cerebellar stroke, bleed, tumor, with imaging 4. Dx rule out meniere’s disease & vestibular migraines- refer to ENT for meniere’s disease

Disequilibrium- ataxia, balance issues, proprioceptive loss, side effects, cervicogenic, postural instability from parkinsonism- teat underlying condition

Any other dizzy sensation? -need a detailed history and neuro exam to evaluate for abnormalities

*Scenario:** A 65-year-old male presents with dizziness and lightheadedness upon standing. He reports that this began a few weeks ago and is more noticeable in the morning. He denies any vertigo or syncope. His medication list includes a diuretic for hypertension. **Question:** What would be the most appropriate initial step to evaluate this patient's dizziness? - A) Dix-Hallpike maneuver - B) Orthostatic vital signs - C) MRI of the brain - D) Referral to a cardiologist

*Answer:** B) Orthostatic vital signs **Rationale:** Orthostatic hypotension commonly presents with dizziness or lightheadedness upon standing. Checking orthostatic vital signs (measurements taken while the patient is lying, sitting, and standing) can help determine if a significant drop in blood pressure when changing positions is contributing to symptoms.

A 40-year-old woman reports episodes of spinning sensation lasting a few seconds when she turns her head a certain way. She has no hearing changes or neurologic symptoms. **Question:** Which maneuver would be most appropriate to perform based on her symptoms? - A) Epley maneuver - B) Dix-Hallpike maneuver - C) HINTS exam - D) Audiometry evaluation

**Answer:** B) Dix-Hallpike maneuver **Rationale:** The Dix-Hallpike maneuver is used to diagnose Benign Paroxysmal Positional Vertigo (BPPV), which typically presents as brief episodes of vertigo provoked by head movements. This maneuver can elicit nystagmus characteristic of BPPV.

A 50-year-old man presents with persistent vertigo and nausea that started suddenly two days ago. He has no hearing loss or other neurological symptoms. Physical exam reveals normal coordination and gait. **Question:** What combination of tests might you use to help differentiate peripheral vertigo from a central cause? - A) Audiometry and Dix-Hallpike maneuver - B) MRI of the brain and orthostatic vital signs - C) HINTS exam - D) Epley maneuver and referral to ENT

Answer:** C) HINTS exam **Rationale:** The HINTS exam (Head-Impulse, Nystagmus, Test of Skew) is a series of bedside tests used to differentiate peripheral causes of vertigo (like labyrinthitis or vestibular neuritis) from central causes (such as brainstem or cerebellar stroke). A reassuring HINTS exam (showing peripheral findings) can often preclude the need for immediate imaging.

A 47-year-old woman has episodic vertigo, tinnitus, and fluctuating hearing loss. Her symptoms have been persisting over several months and disrupt her daily living. **Question:** Which referral or management strategy is appropriate for her condition? - A) Initiate meclizine and observe for several months - B) Urgent MRI to rule out brain tumor - C) Referral to an ENT specialist - D) Immediate initiation of vestibular rehabilitation

Answer:** C) Referral to an ENT specialist **Rationale:** The combination of episodic vertigo, tinnitus, and hearing loss suggests Meniere's disease. Management often includes lifestyle adjustments, potential medical therapy, and sometimes surgical intervention. An ENT specialist can provide specific evaluation and management particular for Meniere's disease.

A 35-year-old male presents with sudden onset vertigo, vomiting, and difficulty walking. He is diagnosed with vestibular neuritis. **Question:** What initial pharmacologic treatment would be appropriate to alleviate his symptoms? - A) Beta-blocker - B) Metoclopramide - C) Meclizine - D) Diuretic

Answer:** C) Meclizine **Rationale:** Meclizine is an antihistamine used to help reduce the spinning sensation and nausea associated with peripheral vertigo conditions such as vestibular neuritis. It acts primarily as a vestibular suppressant and can provide symptomatic relief.

HINTS examination?

A three-step physical examination technique used to clinically differentiate between peripheral and central causes of acute vestibular syndrome. Consists of a head impulse test, evaluation of nystagmus, and a test of skew. Peripheral causes have a positive head impulse test, unidirectional horizontal nystagmus, and a negative test of skew. A central cause is suspected if any of the following are present: vertical, torsional, or direction-changing nystagmus, a negative head impulse test, or a positive skew deviation test.

Central vertigo?

normal head impulse test, any central-type nystagmus (e.g., direction-changing, vertical, or torsional nystagmus), AND/OR skew deviation

peripheral vertigo?

abnormal head impulse test, only peripheral-type nystagmus (e.g., spontaneous unidirectional horizontal nystagmus), AND no skew deviation

Obtain immediate neuroimaging to evaluate for central causes in patients with acute vertigo and focal neurological deficits and/or abnormal HINTS testing, especially if risk factors for ischemic stroke are present.

Clinical findings of central vertigo?

focal neuro deficits- hemiplegia, lateralized facial weakness, focal sensory deficits, and dysfunction of speech, vision, and hearing. severe headache HINTS exam= central vertigo Risk factors for ischemic stroke A collection of patient factors that increase the risk of ischemic stroke. Traditionally classified as either nonmodifiable (e.g., age ≥ 65 years, male sex, genetic factors, minority groups) or modifiable risk factors (e.g., hypertension, hyperlipidemia, cardiovascular disease, diabetes mellitus, alcohol and/or tobacco use).

MRI of the brain next step for ?

central vertigo

____ is indicated if clinical findings raise suspicion for a central cause of vertigo (e.g., cerebellar stroke, lateral medullary syndrome), especially in patients with any risk factors for ischemic stroke (e.g., age ≥ 65 years, multiple comorbidities).

neuroimaging

Vertical nystagmus can indicate?

stroke

__-_ is often acute in onset, may be milder, and is characterized by persistent symptoms. The presence of other neurologic abnormalities on examination — including cranial-nerve abnormalities, motor or sensory changes, and dysmetria or ataxia — suggests a diagnosis of central vertigo. Nystagmus that changes direction with gaze and persists with visual fixation raises suspicion for a central etiology. Nystagmus resulting from a central etiology may be horizontal, vertical, or torsional. Vascular risk factors such as hypertension and diabetes mellitus should also raise suspicion for a central etiology, such as transient ischemic attack or stroke.

central vertigo

___ is also frequently acute in onset, especially in the case of benign paroxysmal positional vertigo (BPPV). The nystagmus seen with peripheral vertigo typically suppresses with visual fixation and often does not change direction with changing gaze. A history of recurrent brief episodes of vertigo — and vertigo and mixed torsional and upbeat nystagmus elicited by the Dix-Hallpike maneuver — is consistent with BPPV.

peripheral vertigo

____ exam or stroke in acute vestibular syndrome can be helpful in differentiating central versus peripheral etiologies of vertigo in the acute phase. The examination consists of the three components detailed below and is valid only when the patient is actively experiencing vertigo.

HINTS * Head Impulse: With the patient’s gaze fixed on an object in the distance, quickly turn the patient’s head 10 degrees in either direction. A normal result is the absence of catch-up saccade, which is also found in central vertigo. A corrective saccade (eyes turning with head and then returning to the distant object) is expected with peripheral causes. * Nystagmus: Vertical, torsional, and bidirectional nystagmus suggests a central cause. Spontaneous unidirectional horizontal nystagmus suggests a peripheral cause. * Test of Skew: With the patient looking straight ahead, alternate between covering and uncovering each eye. A vertical change in position of a covered eye after being uncovered is abnormal and suggests a central lesion. Key learning point: Direction-changing nystagmus that does not suppress with visual fixation is a feature that suggests a diagnosis of central vertigo.

A history of recurrent brief episodes of vertigo — and vertigo and mixed torsional and upbeat nystagmus elicited by the Dix-Hallpike maneuver — is consistent with?

is consistent with BPPV.

A symptomatic triad of peripheral vertigo, tinnitus, and sensorineural hearing loss.

Characteristic of Ménière disease.

Consider short-term symptomatic pharmacotherapy with vestibular suppressants (e.g, first-generation antihistamines, benzodiazepines, antiemetics). Consider movement restriction.

Chronic use of vestibular suppressants is contraindicated because of their potential to inhibit central compensation, which could elicit gait and postural instability.

Dislodged otoliths can cause the severe vertigo attacks seen in benign paroxysmal positional vertigo (BPPV). When otoliths become displaced into one of the semicircular ducts, they can disrupt the endolymph and thus lead to stimulation of the hair cells on the cupula. This stimulation sends signals to the brain that suggest motion even if the patient is not moving, thus triggering the sensation of vertigo. Although this patient has vertigo, she also has cochlear symptoms (tinnitus and hearing loss), which are typically absent in BPPV. Additionally, contrary to this patient's presentation, vertigo in BPPV lasts only for a few seconds and is triggered by movement.

Reduced resorption of endolymph leads to the accumulation of fluid in the endolymphatic sac and causes Meniere disease. If an audiometry was performed, it would typically show low-frequency hearing loss, which can be a helpful finding in differentiating Meniere disease from other conditions that manifest with hearing loss in other frequency ranges (e.g., acoustic neuroma).

As there is no definitive cure for Meniere disease, treatment is directed toward symptomatic management and prevention of recurrence. Lifestyle modifications such as stress reduction, a low-sodium diet, and identification and avoidance of triggers (e.g., caffeine, alcohol, nicotine) are part of the initial nonpharmacological treatment for this condition. Further treatment options include vestibular rehabilitation therapy as well as chronic pharmacotherapy (e.g., diuretics) for patients with frequently recurring episodes. Interventional therapy (e.g., chemical vestibular ablation with intratympanic gentamicin, intratympanic steroids) and surgical vestibular ablation (e.g., labyrinthectomy, vestibular neurectomy) are reserved for patients with intractable symptoms that significantly impact their quality of life. Acute episodes of Meniere disease can be treated with vestibular suppressants (e.g., benzodiazepines, first-generation antihistamines).

which results in endolymph accumulation within the membranous labyrinth, is the underlying mechanism of Ménière disease. In addition to vertigo, tinnitus, and sensorineural hearing loss, patients often have ear fullness and nystagmus that can be directed towards the affected side (irritative nystagmus) or the healthy side (reversed nystagmus).

The triad of vertigo, tinnitus, and sensorineural hearing loss (normal Rinne test, lateralization to the unaffected side) is characteristic of Ménière disease.

Repeated exposure to sounds above a threshold of 85 dB (e.g., motorcycle) or a single exposure to sounds above 120 dB (e.g., gunshots, jet takeoffs) can lead to noise-induced hearing loss. Sensorineural hearing loss is caused by irreversible damage to the stereocilia of the hair cells in the organ of Corti. Deployed military personnel, like this patient, have a high occupational risk of developing noise-induced hearing loss. Such hearing loss is slowly progressive and affects high frequencies (3–4 kHz) first, which results in difficulty hearing in crowded environments. Tinnitus is often an associated symptom. There is no definitive treatment available (besides hearing aids); therefore, prevention with appropriate hearing protection is essential. In addition to sensorineural hearing loss, exposure to sudden noise louder than 120 dB can cause conductive hearing loss through rupture of the tympanic membrane. Hearing loss is a risk factor for depressive disorders, which are common among veterans.

This patient’s history and physical examination are consistent with Meniere disease, a relatively uncommon condition that typically manifests in the fourth or fifth decade of life. Classic symptoms include recurrent episodes of true vertigo accompanied by unilateral hearing loss, tinnitus, and aural fullness. Audiologic evaluation during or soon after episodes of vertigo can be helpful in confirming the diagnosis when Meniere disease is suspected. Imaging may be performed to rule out alternate diagnoses, such as MRI of the brain to rule out vestibular schwannoma. Hearing loss in Meniere disease is typically sensorineural on the affected side, consistent with the Weber and Rinne screening results in this case. The hearing loss is typically most severe in the low-to-middle frequencies. Head-impulse, nystagmus, and test-of-skew (HINTS) testing is indicated in cases of vertigo to rule out central causes of the vertigo, such as stroke, intracranial tumors, and brain infections. This patient’s HINTS results are normal, indicating a peripheral cause of her vertigo. Key learning point: Meniere disease results from endolymph buildup in the inner ear, causing recurrent episodes of vertigo accompanied by low-frequency sensorineural hearing loss, tinnitus, and a sensation of aural fullness.

Benign paroxysmal positional vertigo (BPPV) is a common disorder of the inner ear thought to be caused primarily by otoconia (canaliths) dislodging and migrating into one of the semicircular canals, most commonly the posterior semicircular canal, where it disrupts the endolymph dynamics. BPPV is the most common cause of peripheral vertigo. T

Episodic vertigo (spinning sensation) Sudden (“paroxysmal”) and recurrent episodes Lasts several seconds (typically ≤ 1 minute) Triggered by certain head movements (positional vertigo) after a latency of a few seconds. Associated with: Nystagmus Risk of falls and subsequent injury Nausea and vomiting Triggers: Quick rotation of the head relative to gravity is the main trigger of BPPV (see ''Pathophysiology'' section). Lying down, reclining, or standing up quickly Rolling over in bed Bending forwards Suddenly jerking the head to look up or down

BPPV does not typically cause cochlear (e.g., hearing loss or tinnitus) or neurological symptoms.

Dix-Hallpike maneuver [1][7] Indication First-line test for suspected BPPV Gold standard test to diagnose suspected posterior semicircular canal BPPV Suspected anterior semicircular canal BPPV Procedure Ask the patient to sit upright on the examination bed and to keep their eyes open during the procedure. Rotate the head by 45° towards the affected side. Keeping the neck rotated, quickly lay the patient in a supine position with the neck slightly extended (approx 20°) and the affected ear held down at 45°. Hold this position for 20–30 seconds. Examine the eyes for nystagmus Inquire if the patient is experiencing vertigo Wait for resolution of nystagmus and vertigo Slowly reposition the patient into an upright posture with neck in neutral position and observe for reversal of nystagmus. If negative (that is, no nystagmus/vertigo), repeat the maneuver with the head turned to the unaffected side in step 2. Characteristic findings Positive Dix-Hallpike test: positional vertigo and nystagmus triggered during the maneuver Direction of nystagmus Posterior canal BPPV: upbeat nystagmus with ipsiversive torsional nystagmus component Anterior canal BPPV: downbeat nystagmus with ipsiversive torsional nystagmus Further steps Positive test: Perform Epley repositioning maneuver.

What is the Epley positional maneuver?

A method for treating benign paroxysmal positional vertigo (BPPV) by removing the otoliths from the semicircular canals using gravity and targeted movement. Helps to treat BPPV

A 62-year-old woman presents to your clinic complaining of brief episodes of vertigo lasting about 30 seconds, triggered whenever she looks up or rolls over in bed. She denies any hearing loss or tinnitus. **Question 1:** Based on this information, which condition is most likely responsible for her symptoms? - A) Meniere's disease - B) Vestibular neuritis - C) Benign Paroxysmal Positional Vertigo (BPPV) - D) Labyrinthitis

Answer 1:** C) Benign Paroxysmal Positional Vertigo (BPPV) **Rationale:** BPPV is characterized by transient episodes of vertigo triggered by changes in head position relative to gravity, such as looking up or rolling over in bed. The lack of hearing loss or tinnitus further supports the diagnosis of BPPV.

Which diagnostic test would be best to confirm your suspected diagnosis of BPPV in this patient? - A) Audiogram - B) Electronystagmography - C) Dix-Hallpike maneuver - D) Romberg test

Answer 2:** C) Dix-Hallpike maneuver **Rationale:** The Dix-Hallpike maneuver is the standard test used to diagnose BPPV. It involves moving the patient into a position where gravity can move any dislodged otoconia in the semicircular canals, often triggering nystagmus and vertigo if BPPV is present.

Following a positive Dix-Hallpike test that reproduces her vertiginous symptoms, you confirm the diagnosis of BPPV. **Question 3:** What is the most appropriate initial management for this patient? - A) Prescribe an antihistamine such as meclizine - B) Advise bed rest for 48 hours - C) Perform a canalith repositioning maneuver, such as the Epley maneuver - D) Recommend daily vestibular rehabilitation exercises

Answer 3:** C) Perform a canalith repositioning maneuver, such as the Epley maneuver **Rationale:** The Epley maneuver is the most effective initial treatment for BPPV as it is designed to move canaliths (otoconia) out of the semicircular canal where they are causing symptoms back to the utricle.

If the canalith repositioning maneuver is unsuccessful, what should be the next step for managing persistent BPPV symptoms? - A) Refer the patient to a neurologist - B) Start vestibular suppressant medications - C) Repeat the maneuvers or consider additional vestibular rehabilitation therapy - D) Perform surgical intervention

Answer 4:** C) Repeat the maneuvers or consider additional vestibular rehabilitation therapy **Rationale:** If initial canalith repositioning therapy is not successful, it may be repeated, and vestibular rehabilitation therapy can be considered as an adjunct to improve symptoms and balance. Surgical interventions are rare and typically reserved for cases where all other treatments have failed.

The combination of positional vertigo, normal hearing, and a positive Dix-Hallpike maneuver demonstrating rotary and/or up-beating nystagmus with latency and fatigability is most consistent with a diagnosis of benign paroxysmal positional vertigo. Key learning point: The findings of positional vertigo, normal hearing, and a positive Dix-Hallpike maneuver demonstrating rotary and/or up-beating nystagmus with latency and fatigability are most consistent with a diagnosis of benign paroxysmal positional vertigo.

can be caused by head trauma; vertigo and nystagmus are brief and prompted by movement. A thorough history is crucial because imaging is usually uninformative and formal vestibular testing is less available. A bedside Dix-Hallpike test is easy to conduct. BPPV that involves the posterior canal, which is the most common type, manifests with a prominent rotatory (torsional) nystagmus with a minor vertical (up-beating) component. Key learning point: The most likely diagnosis in a patient with head trauma followed by nausea, vomiting, positional vertigo, and prominent rotatory nystagmus is benign paroxysmal positional vertigo.

is a common disorder that manifests as brief (10- to 20-second) episodes of intense vertigo provoked by certain changes in head position or gaze. There are no focal neurological deficits on examination. The diagnosis is established with the help of the Dix-Hallpike maneuver. With the patient sitting upright, the head is rotated approximately 45 degrees to the patient’s right. The patient is then helped to lie down quickly on their back with their head held in approximately 20 degrees of extension. This is usually done with the patient’s head hanging off the examination table, and their eyes are observed. The test is considered positive for BPPV when there is a 2- to 10-second period of latency before the onset of rotational nystagmus, which would be upbeat and torsional, with the top poles of the eyes beating toward the lower (right) ear. When the patient sits back up, the nystagmus will often reverse direction in cases of BPPV involving the posterior semicircular canal. Key learning point: A diagnosis of benign paroxysmal positional vertigo can be established definitively using the Dix-Hallpike maneuver, which involves observing for nystagmus after placing the head in extension and rotating it 45 degrees.

is characterized by brief episodes of vertigo provoked by a change in head position. It is caused by free-floating particulate matter (canaliths) in the endolymph of the semicircular canal. In patients with posterior canal BPPV (the most common subtype of BPPV), a Dix-Hallpike maneuver triggers vertigo and, typically, mixed torsional and upbeat nystagmus, with the upper pole of the eye beating toward the dependent ear and the upbeat nystagmus beating toward the forehead. The recommended treatment for posterior canal BPPV is the Epley maneuver, which helps reposition the canaliths into the vestibule of the semicircular canal where they can be resorbed. In this maneuver, the patient is moved from a seated to a supine position with the head rotated 45 degrees toward the right and the neck slightly extended, followed 30 seconds later by slow rotation of the head until the left ear is facing down, followed 30 seconds later by further rotation of the head and body to the left. Then the patient is returned to a seated position. Key learning point: The first-line treatment for benign paroxysmal positional vertigo is the Epley maneuver.

and stroke are the two most common causes of unilateral facial weakness. In this case, the patient has unilateral weakness of both the upper and lower face, which strongly suggests a peripheral lesion. Although the eyes and forehead receive innervation from both cerebral hemispheres, the lower face receives innervation only from the contralateral hemisphere. A single cerebral lesion would not cause weakness of the entire side of the face. Although facial nerve palsy can be caused by infection, autoimmune disease, tumors, and other processes, it is most often idiopathic. Bell palsy is fairly common, with an annual incidence of 20 cases per 100,000 people. Treatment for Bell palsy consists of a short course of oral glucocorticoids, which has been shown in multiple trials to increase the likelihood of complete recovery of facial function. In clinical practice, glucocorticoids are often combined with an antiviral agent (acyclovir, valacyclovir, or famciclovir) based on evidence suggesting that this combination can improve outcomes further, but the quality of the studies supporting this approach was hampered by trial design. If this patient had signs or symptoms of ear involvement or a rash consistent with Ramsay Hunt syndrome (vesicles in the auditory canal or pinna), valacyclovir treatment would be much more likely to be beneficial. Key learning point: Glucocorticoids increase the likelihood of complete recovery of facial function in patients with Bell palsy.

Bells palsy treatment - oral prednisone for 10 days

A patient who reports mild chronic bilateral conjunctivitis and pain with urination most likely has chlamydial conjunctivitis resulting from autoinoculation. Chlamydia trachomatis, a common cause of chronic indolent conjunctivitis, is associated with injection, mucus discharge, preauricular lymph-node enlargement, follicles on the inferior tarsal conjunctiva, and a history of urethritis, cervicitis, or vaginitis. C. trachomatis infections are diagnosed using conjunctival culture, DNA probe, or microscopic examination. C. trachomatis infections are generally treated with oral antibiotics, preferably azithromycin or doxycycline. Topical antibiotic ointments, such as erythromycin or tetracycline, can be used as adjunctive therapy. Chlamydia trachomatis serotypes that cause urethritis and chronic conjunctivitis are different than the ones that cause endemic trachoma. Endemic trachoma is seen in resource-limited settings and is rare outside the developing world. In a patient with conjunctivitis, urethritis, and arthritis, the diagnosis of reactive arthritis should be entertained. In this particular case, the patient did not report arthritis or photophobia, which would be a sign of concomitant uveitis. Key learning point: A patient with mild chronic conjunctivitis and pain with urination most likely has a diagnosis of chlamydial conjunctivitis.

Contact lens wearers are at increased risk of serious infections with gram-negative bacteria such as Pseudomonas aeruginosa.

Commonly used classes of antibiotics in children and adults include : Macrolides, e.g., erythromycin or azithromycin Combination drops, e.g., polymyxin B/trimethoprim Fluoroquinolones, e.g., ciprofloxacin (use if gram-negative pathogens are suspected, e.g., in contact lens wearers) Sulfonamides, e.g., sulfacetamide Aminoglycosides, e.g., tobramycin

The finding of gram-negative intracellular diplococci in a patient with clinical features of bacterial meningitis is indicative of infection with Neisseria meningitidis. Although the incidence of such infection is decreasing as a result of multiple factors, including routine use of meningococcal vaccine, N. meningitidis can cause rapidly progressive acute bacterial meningitis and septicemia. The most common cause of spread from one individual to another is through short-range aerosolized oral secretions, which makes close quarters such as summer camps and college dormitories uniquely prime environments for transmission. The Centers for Disease Control and Prevention, as well as the American Academy of Pediatrics, recommend postexposure chemoprophylaxis for individuals who have been exposed to patients with a known or presumed diagnosis of N. meningitidis infection. Such individuals include: * Those who have had contact with the patient’s oral or respiratory secretions, such as through kissing, mouth-to-mouth resuscitation, endotracheal tube intubation, and endotracheal tube care * Household members, day-care contacts, and anyone who has spent extensive time close to the patient within the 7 days before symptom onset * Travelers who have sat directly next to the index patient on an airline flight lasting longer than 8 hours First-line chemoprophylaxis for a child exposed to a patient with N. meningitidis infection is oral rifampin. Alternatives include ciprofloxacin and ceftriaxone. Each of these agents is 90% to 95% effective in eliminating nasopharyngeal carriage of N. meningitidis. When rifampin is used, it should ideally be initiated within 24 hours after exposure; the appropriate dose is 10 mg/kg (maximum 600 mg) every 12 hours for 2 days for a total of 4 doses. When ciprofloxacin or ceftriaxone is used, it is administered as a single dose following exposure. Key learning point: The appropriate prophylaxis for a child exposed to a household member with Neisseria meningitidis infection is oral rifampin, ideally administered within 24 hours after exposure.

In adults with suspected bacterial meningitis, empiric ceftriaxone and vancomycin should be administered immediately to cover the most common etiologic agents; dexamethasone is also administered in most patients with suspected meningitis, given evidence showing a reduction in neurologic sequelae among patients with pneumococcal meningitis who received dexamethasone. Empiric addition of ampicillin is recommended for treatment of bacterial meningitis in people > 50 years of age. Ampicillin or penicillin is the preferred agent for treating L. monocytogenes infections. Synergy with aminoglycosides, such as gentamicin, has been demonstrated in vitro, and these agents are often used in conjunction with penicillins in treating Listeria meningitis.

In most patients with suspected bacterial meningitis, a lumbar puncture can be done without any preceding head imaging. However, not all patients can proceed directly to a lumbar puncture. This procedure carries a risk of brain stem herniation and death in those with elevated intracranial pressure; thus, patients at risk for elevated intracranial pressure should undergo head imaging before proceeding to lumbar puncture. This includes patients who present with a seizure (as in this case), those with focal neurologic deficits, those who are immunocompromised, and those with evidence of papilledema or a moderate-to-severely impaired level of consciousness. In most settings, CT is the most readily available test for brain imaging. MRI provides similar information, but it takes longer and may result in delays to other diagnostic and therapeutic interventions.

This patient has acute bacterial meningitis, most likely caused by Streptococcus pneumoniae. In acute bacterial meningitis, the CSF is typically cloudy with a neutrophil-predominant pleocytosis, elevated protein levels, and lowered glucose, with the CSF-to-plasma glucose ratio < 0.4. S. pneumoniae is the most common cause of bacterial meningitis in older adults; it appears as gram-positive lancet-shaped diplococci on Gram stain. Because of the risk of ceftriaxone-resistant strains of S. pneumoniae, current guidelines recommend that patients with meningitis caused by S. pneumoniae be treated with a combination of vancomycin and ceftriaxone while susceptibility results are pending. In addition, a systematic review of five studies involving adults with acute bacterial meningitis showed that adjunctive dexamethasone reduced mortality risk in patients with pneumococcal meningitis. Typically, a 4-day course of intravenous dexamethasone 10 mg every 6 hours is recommended. Ampicillin is recommended as empiric treatment for Listeria monocytogenes meningitis in immunocompromised people and in adults aged 50 years and older; however, Listeria typically appears as slender gram-positive bacilli on Gram stain. Key learning point: In a patient with suspected Streptococcus pneumoniae meningitis, the most appropriate regimen tonitiate while awaiting antibiotic susceptibilities consists of dexamethasone plus both vancomycin and ceftriaxone.

Hypotension, hyperkalemia, and hyponatremia in a critically ill patient are consistent with a diagnosis of acute adrenal insufficiency.

In cases of suspected bacterial meningitis, the most important determinant of outcome is timely initiation of antibiotics after collection of blood and cerebrospinal fluid for culture and analysis.

The most appropriate empiric treatment for an adult with suspected acute bacterial meningitis consists of a third-generation cephalosporin, such as ceftriaxone, which covers the most common causes of bacterial meningitis in adults; vancomycin, which covers possible beta-lactam-resistant Pneumococcus; and adjunctive dexamethasone, which has been shown to improve outcomes.

The most appropriate sequence for evaluation and treatment in a stable child with suspected bacterial meningitis and an open, bulging fontanelle is to draw blood, perform a lumbar puncture, and treat with empiric antibiotics and dexamethasone.

There are four types of hearing loss: * Conductive hearing loss involves reduced transmission of sound through the external and middle ear. * Sensorineural hearing loss involves an inability to transduce vibrations to neural impulses within the cochlea or to transmit neural impulses through the vestibulocochlear nerve. * Mixed hearing loss is a combination of conductive and sensorineural hearing loss. * Central hearing loss involves defects in the brainstem or auditory processing centers of the brain. This patient had a normal hearing test shortly after birth and now, at age 3, has evidence of mild bilateral sensorineural hearing loss. Bacterial meningitis is the most common cause of acquired sensorineural hearing loss and is the most likely cause in this case. Although the hearing loss associated with bacterial meningitis typically occurs early in infection, it can also manifest later and be progressive. For this reason, all patients with bacterial meningitis should have a hearing evaluation within 4 to 8 weeks after hospital discharge and then 6 to 12 months later. Key learning point: The most common cause of acquired sensorineural hearing loss in children is bacterial meningitis.

with meningitis, whether bacterial or viral, typically present with fussiness, vomiting, and (in older children) nuchal rigidity. Cerebrospinal fluid (CSF) analysis is crucial to distinguish bacterial from viral disease. CSF pleocytosis with a predominance of polymorphonuclear cells, a low glucose level (≤2/3 of the serum value), and an elevated protein level are all suggestive of bacterial meningitis. Streptococcus pneumoniae is the most common cause of bacterial meningitis in infants 3 months of age or older, although the incidence of invasive pneumococcal disease has declined since the pneumococcal conjugate vaccine was introduced. The current pneumococcal vaccine provides protection against the 13 most common invasive serotypes, but cases still occur, and this patient is at increased risk because of incomplete immunizations. Key learning point: In an infant aged 3 months or older whose cerebrospinal fluid profile suggests bacterial meningitis, the most likely causative pathogen is Streptococcus pneumoniae.

is a common complication of meningococcal meningitis in children. In a prospective Canadian study of children with meningococcal meningitis, 21% of those aged 1 to 4 years had hearing loss, as did 19% of those aged 5 to 15 years. Hearing loss is also a common long-term complication of other types of bacterial meningitis and is most commonly seen in pneumococcal meningitis. The hearing loss typically occurs during the acute illness, so all children with bacterial meningitis should be tested for hearing loss at the time of hospital discharge. Clinicians should remain vigilant in screening after discharge as well. Key learning point: Children who are being discharged after a hospitalization for meningococcal meningitis should be screened for hearing loss.

Hearing loss

In children outside the neonatal period, the most common pathogens associated with bacterial meningitis are Streptococcus pneumoniae and Neisseria meningitidis.

Posterior Semicircular Canal BPPV** **Q:** What is the most common diagnostic test for detecting posterior semicircular canal BPPV, and what are its expected findings?

*A:** The Dix-Hallpike test is the most common diagnostic test. Expected findings include up-beating and torsional nystagmus, which is indicative of posterior canal involvement. **Rationale:** The posterior semicircular canal accounts for approximately 85% of BPPV cases. The characteristics of nystagmus during the Dix-Hallpike test help confirm this diagnosis.

Which maneuvers are commonly used to treat posterior semicircular canal BPPV? **A:** The Epley maneuver and the Semont liberatory maneuver.

Rationale:** These maneuvers aim to reposition the dislodged otoconia from the semicircular canal back into the utricle, relieving symptoms of vertigo.

What Dix-Hallpike test findings suggest involvement of the anterior (superior) semicircular canal? **A:** The presence of down-beating and vertical nystagmus during the Dix-Hallpike test indicates anterior canal involvement.

*Rationale:** The specific pattern of nystagmus helps differentiate between types of BPPV, as the anterior canal can cause down-beating nystagmus when provoked.

How is anterior semicircular canal BPPV commonly treated, and what is its natural course?

The Epley maneuver may be used, but this type of BPPV often spontaneously resolves over time. **Rationale:** Spontaneous resolution is typical because otoconia may naturally return to their original location. When treatment is performed, the Epley maneuver can still be effective.

What diagnostic test is used for lateral semicircular canal BPPV, and what form of nystagmus is observed? **A:** The supine head roll test (or Pagnini-McClure maneuver) is used. It typically results in horizontal geotropic or apogeotropic nystagmus.

*Rationale:** The direction of the nystagmus during this test can confirm the involvement of the lateral canal, which behaves differently from the posterior or anterior canals.

What maneuvers are effective in treating lateral semicircular canal (canalithiasis) BPPV? **A:** The Lempert 360-degree roll maneuver (also known as the log roll maneuver) and the Gufoni maneuver.

Rationale:** These maneuvers are specifically designed to address particle movement in the horizontal canal, relieving the symptoms associated with lateral canal BPPV.

who do you refer for BPPV?

ENT, Audiologist, PT

What are the meds to treat symptoms?

dizziness- dramamine, meclisine nausea/vomitting- phenergan, zofran

dimenhydrinate (dramamine) (BPPV)

antihistamine for preventing/treating motion sickness, nausea, vomiting, dizziness anticholinergic effects CNS depression decreases central histamine effects ototoxicity tachycardia may use during pregnancy; risk of fetal harm not expected based on limited human data

meclizine (BPPV)

antihistamine, 1st generation Interaction Characteristics: anticholinergic effects CNS depression decreases central histamine effects tachycardia Contraindicated in isocarboxazid- CNS depression potassium chloride- increase risk of GI ulcer potassium citrate- increase risk GI ulcer tranylcypromine---CNS depression

phenergan (promethazine)- BPPV

Black Box Warnings: Respiratory Depression contraindicated in pts <2 yo due to cases of resp. depression, some fatal, at wide-range of wt-based doses; in pts 2 yo and older, use w/ caution at lowest effective dose, avoid combo w/ other resp. depressant drugs Severe Tissue Injury, Gangrene severe chemical irritation and tissue damage, incl. gangrene, tissue necrosis, and thrombophlebitis have occurred regardless of parenteral admin. route; some cases require surgical intervention, incl. fasciotomy, skin graft, and/or amputation; IV injection at conc. >1 mg per mL, intra-arterial injection, and SC injection contraindicated; IM route preferred; if must use IV, dilute through IV catheter inserted in large vein, preferably central venous catheter; immed. D/C if pain occurs, evaluate for possible arterial injection or perivascular extravasation, and initiate appropriate medical management

phenergan (promethazine)- BPPV

Interaction Characteristics: anticholinergic effects CNS depression decreases central histamine effects dopamine antagonist extrapyramidal effects hypotensive effects lowers seizure threshold photosensitivity prolongs QT interval (conditional) Contraindicated cisapride- combo may incr. risk of QT prolongation, cardiac arrhythmias, extrapyramidal sx; may decr. cisapride efficacy (additive effects; antagonistic effects) pimozide-combo may incr. risk of QT prolongation, cardiac arrhythmias, CNS and resp. depression, psychomotor impairment, seizures, extrapyramidal sx, anticholinergic adverse effects (additive effects) potassium chloride- GI ulcer risk potassium citrate- GI ulcer risk thioridazine-combo may incr. risk of QT prolongation, cardiac arrhythmias, hypotension (incl. orthostasis), CNS and resp. depression, psychomotor impairment, seizures, anticholinergic adverse effects (additive effects; duplicate tx) Monitoring Parameters CBC w/ diff, ophthalmic exam if prolonged tx may use during pregnancy; risk of fetal harm low, Lactation may use short-term while breastfeeding,

zofran (BPPV treatment) ondansetron

Contraindicated apomorphine- combo may result in profound hypotension, loss of consciousness; may incr. risk of QT prolongation, cardiac arrhythmias (mechanism unknown; additive effects) cisapride- combo may incr. risk of QT prolongation, cardiac arrhythmias (additive effects) dofetilide-- combo may incr. dofetilide levels, risk of QT prolongation, cardiac arrhythmias, other adverse effects (renal transport inhibited, additive effects) domperidone- combo may incr. risk of QT prolongation, cardiac arrhythmias (additive effects) dronedarone- combo may incr. risk of QT prolongation, cardiac arrhythmias (additive effects) levoketoconazole- combo may incr. risk of QT prolongation, cardiac arrhythmias (additive effects) pimozide- combo may incr. risk of QT prolongation, cardiac arrhythmias (additive effects) thioridazine-combo may incr. risk of QT prolongation, cardiac arrhythmias (additive effects) ondansetron 5-HT3 antagonist Interaction Characteristics: CYP3A4 substrate MATE1 inhibitor MATE2-K inhibitor OCT2 inhibitor prolongs QT interval (known) serotonergic effects

When should you refer to a neurologist for headache treatment?

-increase frequency and severity of unilateral headaches -atypical auras -changes in personality -excessive sleepiness -new onset deficitis **can be mass lesion, hemorrhage, or structural disorder