1. VERTIGO NOT JUST DIZZINESS
Lafe Bush

2. Definition's Vertigo Dizziness
An abnormal sensation of movement or rotation of the patient or their environment
Dizziness
Is a range of sensations such as feeling faint, woozy, weak or unsteady, Lightheaded, or pre syncope
Vertigo is defined as a pathologic illusion of movement or a feeling of movement when no movement exists. 6 Most commonly experienced as a spinning sensation, it arises from a pathologic imbalance in the peripheral or central vestibular system. Patients will often merely report feeling dizzy, and further questioning is required to identify vertigo.7 Caution is advised in classifying the dizzy patient. While differentiating vertigo from imbalance, presyncope and lightheadedness was traditionally taught, studies show that patients use overlapping terms to describe their experience and even change their minds during a single clinical encounter.8 The best way for a clinician to identify a vertigo syndrome is to realize that while most patients will report the classic rotational vertigo, approximately 17% will not.9 These patients may report episodic imbalance or dizziness that is made worse with head movement.

3. Vertigo Affects 20-30% of the population 2.5% of all ED visits
2-3 times more common in women then men

4. PREVELENCE of DIZZYNESS
Common DX
32.9% otologic/vestibular
21.1% cardiovascular
11.5% respiratory
11.2% neurologic (4% CVA)
11% metabolic
10.6% injury/poisoning
7.2% digestive
According to this study 32.6% had a serious medical condition that needed to be addressed.

5. Anatomy

6. VASCULATURE OF THE BRAIN
Right/Left common carotid arteries
External = face and scalp
Internal = anterior 3/5 of cerebrum
Right/left vertebral arteries
2/5 cerebrum, cerebellum, and brainstem
Circle of Willis
Anterior cerebral artery
Middle cerebral artery
Posterior cerebral artery
Circle of Willis
At the base of the brain, the carotid and vertebrobasilar arteries form a circle of communicating arteries known as the Circle of Willis. From this circle, other arteries—the anterior cerebral artery (ACA), the middle cerebral artery (MCA), the posterior cerebral artery (PCA)—arise and travel to all parts of the brain. Posterior Inferior Cerebellar Arteries (PICA), which branch from the vertebral arteries, are not shown.
Because the carotid and vertebrobasilar arteries form a circle, if one of the main arteries is occluded, the distal smaller arteries that it supplies can receive blood from the other arteries (collateral circulation).
Anterior Cerebral Artery
The anterior cerebral artery extends upward and forward from the internal carotid artery. It supplies the frontal lobes, the parts of the brain that control logical thought, personality, and voluntary movement, especially of the legs. Stroke in the anterior cerebral artery results in opposite leg weakness. If both anterior cerebral territories are affected, profound mental symptoms may result (akinetic mutism)
Middle Cerebral Artery
The middle cerebral artery is the largest branch of the internal carotid. The artery supplies a portion of the frontal lobe and the lateral surface of the temporal and parietal lobes, including the primary motor and sensory areas of the face, throat, hand and arm, and in the dominant hemisphere, the areas for speech.
The middle cerebral artery is the artery most often occluded in stroke.
Posterior Cerebral Artery
The posterior cerebral arteries stem in most individuals from the basilar artery but sometimes originate from the ipsilateral internal carotid artery [Garcia JH et al., In Barnett HJM at al (eds) Stroke Pathophysiology, Diagnosis, and Management New York Churchill Livingstone ]. The posterior arteries supply the temporal and occipital lobes of the left cerebral hemisphere and the right hemisphere. When infarction occurs in the territory of the posterior cerebral artery, it is usually secondary to embolism from lower segments of the vertebral basilar system or heart.
Clinical symptoms associated with occlusion of the posterior cerebral artery depend on the location of the occlusion and may include thalamic syndrome, thalamic perforate syndrome, Weber’s syndrome, contralateral hemplegia, hemianopsia and a variety of other symptoms, including including color blindness, failure to see to-and-fro movements, verbal dyslexia, and hallucinations. The most common finding is occipital lobe infarction leading to an opposite visual field defect.

7. Cranial Nerves

8. Vestibular Apparatus Vestibular nerve 3 Semi Circular Canals Macula
Sends messages to the brain
3 Semi Circular Canals
Filled with fluid which moves and gives information about speed and direction
Macula
Located in the Vestibule Contains hair cells (Crista) with give information about the position of the head
Otoliths cristals located in Macula

9. Posterior canal detects when the head moves towards the shoulder
Superior detects when the head nods up and down in the yes motion
Lateral detects when the head goes right to left in yes and no motion

10. CLASSIFICATIONS OF VERTIGO
Central Vertigo
Due to a disease process of the central nervous system
Peripheral Vertigo
Disorders of the inner ear and/or 8th cranial nerve

11. CENTRAL VERTIGO Stroke Tumors Vertebrobasilar Disease Intoxications
Multiple Sclerosis
Migraines

12. Differentiation Central Vertigo
Vertigo lasting hours to days
Less severe then with peripheral vertigo
Relatively unaffected by head movement
Nausea/Vomiting
Unsteady Gait
Unable to sit upright with arms crossed
Finger to nose test/heel to knee test
Past Medical History

13. PMH ASSOCIATED WITH CENTRAL VERTIGO
Hypertension
Atrial Fibrillation
Cardiac embolism
Valvular problems
History of CVA
Obesity
Atherosclerosis
Diabetes
Sickle cell anemia

14. STROKE’s Cerebellar infarction
Posterior inferior cerebellar artery syndrome
Cerebellar and brainstem hemorrhage

15. CEREBELLUM Supplied by Superior Cerebellar Artery (SCA)
Anterior Inferior Cerebellar Artery (AICA)
Posterior Inferior Cerebellar Artery (PICA)

16. Cerebellar strokes 1.5% of all strokes
10% of all cerebellum strokes will be a cerebellar hemorrhage
Commonly missed diagnoses in the ED and pre-hospital setting

17. S &S Cerebellar Strokes
Vertigo
Dyscoordination
Gait Ataxia
Nose finger test
Running the heal of foot down shin
Ability to walk
Ability to sit up straight with arms crossed

18. VERTEBROBASILAR INSUFFICIENCY
Vertigo
Loss of vision
Diplobia
Nausea/vomiting
Loss of coordination
Vertebrobasilar insufficiency is a condition characterized by poor blood flow to the posterior (back) portion of the brain, which is fed by two vertebral arteries that join to become the basilar artery. Blockage of these arteries occurs over time through a process called atherosclerosis, or the build-up of plaque. Plaques are made up of deposits of cholesterol, calcium and other cellular components. They not only make the arteries ‘hard,’ they grow over time and can obstruct or even block the flow of blood to the brain.
The vertebrobasilar arteries supply oxygen and glucose to the parts of the brain responsible for consciousness, vision, coordination, balance and many other essential functions. Both restricted blood flow and the complete blockage of it — called ischemic events — have serious consequences for brain cells. Ischemia occurs when blood flow to the brain damages cells. An infarction occurs when the cells die. A transient ischemic attack (TIA), or “mini-stroke,” is an ischemic event that results in the temporary loss of brain function. If the resulting loss of brain function is permanent, it’ s called a stroke (an infarction or brain attack). A stroke can either be caused by blockage in the vertebral or basilar artery or the breaking off of a piece of plaque (embolus) that travels downstream and blocks a portion of the blood flow to the brain.
Basic anatomy The vertebral arteries are branches of the subclavian (upper extremity) arteries. They arise, one on each side of the body, go through the vertebral column (spine) in the back of the neck, and enter the skull via the hole at the base of the skull called the foramen magnum. Inside the skull, the two vertebral arteries join up to form the basilar artery at the base of the medulla oblongata. The basilar artery supplies arterial branches to the brain stem, cerebella and occipital lobes, which control the autonomic nervous system (unconscious functions like breathing, heart rate, etc.), level of conscious, coordination, balance and vision.

19. Posterior inferior cerebellar artery syndrome (Wallenberg’s Syndrome)
Stroke vertebral or posterior inferior cerebellar artery
Supplies blood to the Medulla and Cerebellum
Ipsilateral limb ataxia
Loss of pain and temperature sensation
Vertigo
Feeling of being pulled to one side
Wallenberg’s syndrome is a neurological condition caused by a stroke in the vertebral or posterior inferior cerebellar artery of the brain stem. Symptoms include difficulties with swallowing, hoarseness, dizziness, nausea and vomiting, rapid involuntary movements of the eyes (nystagmus), and problems with balance and gait coordination. Some individuals will experience a lack of pain and temperature sensation on only one side of the face, or a pattern of symptoms on opposite sides of the body – such as paralysis or numbness in the right side of the face, with weak or numb limbs on the left side. Uncontrollable hiccups may also occur, and some individuals will lose their sense of taste on one side of the tongue, while preserving taste sensations on the other side. Some people with Wallenberg’s syndrome report that the world seems to be tilted in an unsettling way, which makes it difficult to keep their balance when they walk.

20. Brain stem Strokes Troublesome due to small size
Symptoms can be one sided or bilateral
Look for crossed signs as nerves cross at the brainstem
Weakness of the arm on left and weakness of the face on right

21. S & S of Brain Stem Strokes
Vertigo
Tenitus
Diplopia
Decrease level of consciousness
Dysarthria
Dysphagia

22. MULTIPLE SCLEROSIS Vertigo lasting hours to weeks
Mild sense of Vertigo
History
Nystagmus will be present
Multiple sclerosis (MS) is a potentially disabling disease of the brain and spinal cord (central nervous system).
In MS, the immune system attacks the protective sheath (myelin) that covers nerve fibers and causes communication problems between your brain and the rest of your body. Eventually, the disease can cause the nerves themselves to deteriorate or become permanently damaged.

23. Migraine 40% of Migraines will be associated with vertigo Vertigo
Dizziness
Unsteadiness
Extreme sensitivity to motion
Aura
Despite being the second most common cause of vertigo seen in clinical practice, migrainous vertigo remains under-recognized.5 Its clinical spectrum can be elusive. Half of patients present without headache.18 Its presenting features can vary, not only among different patients but in the same patient over time. Some have aura while others do not. Some have photophobia during attacks while others do not. For some, the migrainous vertigo appears to be like an aura that lasts for a few minutes (18%), but for others the vertigo lasts for longer than 24 hours (27%).19 Physical examination should reveal a normal neurologic examination, including coordination and gait. Video oculography has demonstrated findings of central nystagmus, but this has not yet been demonstrated on bedside physical examination.20
Formal diagnostic criteria for migrainous vertigo have been proposed.21 Strict criteria require: 1) recurrent episodes of vertigo; 2) a formal migraine diagnosis by International Headache Society (I.H.S.) criteria; 3) a migraine symptom during the attack (e.g. headache, photophobia, or aura); and 4) the exclusion of other causes. The category of “probable migrainous vertigo” is used for patients with some elements in the presentation to suggest migraine but no other identifiable cause.
Cerebellar infarction is not expected to present with migraine-associated symptoms, so most patients with criteria for migrainous vertigo and a normal neurologic examination can be treated for their migraine process without further work-up.

24. PERIPHERAL VERTIGO Vestibular Neuronitis (neuropathy)
Benign paroxysmal positional vertigo
Meniere’s disease
Medications

25. Differentiation Peripheral
Vertigo comes in bursts lasting approximately 30 seconds
Relieved with holding still
One directional nystagmus
Nausea/vomiting

26. Vestibular Neuronitis (neuropathy)
Sudden onset
Debilitating vertigo
Associated unsteadiness
Nausea/vomiting
One directional horizontal nystagmus toward the healthy ear
Vestibular neuritis is characterized by the acute vestibular
syndrome, caused by decreased vestibular tone on one side.
Etiology is currently thought to be viral.22 Vestibular neuritis
is recognized by characteristic findings on history and ocular
examination. The history typically reveals a gradual onset,
unlike for stroke where symptoms reach maximal intensity
at onset. In vestibular neuritis, symptoms peak during the
first day and begin to improve within a few days, although
full recovery takes weeks to months.6
The associated
vertigo is persistent and ongoing, although like all forms of
vertigo, positional exacerbation is characteristic, as any head
movement amplifies the disparity in bilateral vestibular tone.
Associated autonomic symptoms of nausea and vomiting are
prominent.
General neurologic examination is normal, including
motor, sensory, reflexes, cranial nerves and mental status.

27. Benign paroxysmal positional vertigo
Most common cause of vertigo 20%
More common in women
Occurs most often at age 50 or >
Often occurs in the morning when getting out of bed
Benign paroxysmal positional vertigo is a distinct condition not typically confused with cerebellar infarction.
BPPV is a mechanical problem in the inner ear. It occurs when some of the calcium carbonate crystals (otoconia) that are normally embedded in gel in the utricle become dislodged and migrate into one or more of the 3 fluid-filled semicircular canals, where they are not supposed to be. When enough of these particles accumulate in one of the canals they interfere with the normal fluid movement that these canals use to sense head motion, causing the inner ear to send false signals to the brain.
Patients present with brief episodes of intense vertigo, precipitated by a change in position. The paroxysms of intense symptoms lasting less than a minute are defining, as is positional provocation. Patients are well until a head movement, usually vertical, precipitates the paroxysm of symptoms. In most cases BPPV is idiopathic, although 10% follow a bout of vestibular neuritis and 20% follow an episode of head trauma.11
The most common form of BPPV, caused by an otolith in the posterior semicircular canal.

28. BBPV

29. Vestibular Neuritis Viral Gradual onset
Symptoms are worse the first day and then become progressively better
Persistent Vertigo
Labrinthitis is similar but with but with hearing loss or tinnitus

30. Meniere’s disease
Possibly due to a abnormal amount of fluid in the inner ear.
Recurring episodes of vertigo => 20min <24Hours
Nausea Vomiting (severe cases)
Tinnitus (hearing loss over time)
Feeling of fullness in affected side
Meniere’s disease is suspected in the patient who presents with simultaneous vertigo and cochlear complaints. Cochlear complaints can be hearing loss, tinnitus, or aural fullness. Also called endolymphatic hydrops, Meniere’s disease is thought to be caused by a buildup of fluid in the endolymphatic compartment of the inner ear. Episodes commonly last a few hours, although they can range from 20 minutes to a few days. Formal diagnosis requires hearing loss documented on audiologic examination on at least one occasion.14 Patients may have normal audiologic examination between episodes.
It is not common for a stroke to present with isolated vertigo and hearing loss, although case reports do exist.15 It occurs in only 0.3% of all brainstem infarctions and tends to present with complete ipsilateral deafness.16 In general, vertigo with hearing loss, unless it is with total ipsilateral deafness, indicates a peripheral disorder. The clinician should perform a thorough neurologic and neuro-otologic examination on these patients, as discussed below. Patients with a negative work-up for stroke should be referred to an otolaryngologist for further testing and consideration of alternative diagnoses, such as labyrinthitis and schwannoma.6,17 Patients with Meniere’s disease tend to have recurring episodes, so if the patient has not had previous episodes, labyrinthitis should be suspected instead. Labyrinthitis is thought to be the same disease process as vestibular neuritis, with the additional involvement of the auditory system. patients with Meniere’s disease tend to have recurring episodes, so if the patient has not had previous episodes, labyrinthitis should be suspected instead

31. Dizziness
Studies have shown that Vertigo was the primary symptom in 37% of cardiovascular events
55-71% of syncope patients complain of dizziness prior to passing out

32. STROKE SCALES NIH Stroke Scale
Cincinnati Prehospital Stroke Scale (CPSS)
Facial Droop
Arm Drift
Speech
Los Angeles Prehospital Stroke Screen (LAPSS)
Blood Glucose
Grip strength
Arm drift

33. STROKE SCALE CONTINUED
MEND exam
CPSS + NIH

34. NYSTAGMUS Involuntary movement of the eyeballs
Increased blood alcohol levels
Drugs
Strokes
BPVV
And many other reasons

35. Dix-Hallpike maneuver
Rapidly move patient from sitting to supine position with head turned 45 degrees
Wait 30 seconds
Return patient to sitting position
And check for nystagmus (if negative check other side)
Posterior canal BPPV will produce rotational nystagmus towards the lower (affected ear)
Horizontal nystagmus represent horizontal canal involvement
Negative test does not confirm central cause
is diagnosed by finding torsional nystagmus on the Dix-Hallpike test.12 The examiner holds the seated patient’s head 45° to the left or right. This aligns the posterior semicircular canal in the vertical plane. The patient should be asked to hold onto the examiner’s arm for stability. The examiner then drops the patient back to the supine position, with the head hanging down off the stretcher 10°–30°. This causes a large rotation of the posterior semicircular canal within its own plane, moving the loose otolith and reproducing the symptoms. The test is considered positive if it provokes the characteristic torsional and vertical nystagmus.13
The sensitivity of the Dix-Hallpike maneuver for BPPV has not been well-described in the ED setting. Even without a positive Dix-Hallpike test, patients with BPPV can be differentiated from those with cerebellar infarction by their episodic and positional symptoms. Those who do not fit this description require consideration of alternative diagnoses.

36. HEAD IMPULSE, NYSTAGMUS, AND TEST OF SKEW (HINTS)
Horizontal head impulse test
Have patient focus on examiner nose
Rapid low amplitude rotation of the head toward the midline
Eyes should stay focused
In peripheral vertigo rapid movement toward effected side will cause a saccade as they look back at the target (positive)
1 – Patients with peripheral vertigo will have abnormal (positive) head impulse testing, while patients with central vertigo typically have a normal (negative) head impulse test.
Horizontal head impulse testing involves rapid head rotation by the examiner with the subject’s vision fixed on a nearby object (often the examiner’s nose). With rapid low-amplitude rotation of the head toward the midline, the patient’s eyes should remain fixed on the target. In cases of peripheral vertigo, in which the vestibulo-ocular reflex is impaired, rapid rotation of the head toward the affected side will result in loss of fixation and movement of the eyes away from the target. This is followed by a corrective saccade as the subject looks back toward the target. Observation of this corrective saccade is abnormal, and considered a positive test. There is typically no corrective saccade in patients with central vertigo, in whom the vestibulo-ocular reflex usually remains intact. In rare cases of combined stroke and inner ear infarction, patients may have an abnormal head impulse test. In such cases, the central nature of the lesion will be revealed instead by one of three other findings: direction-changing nystagmus, skew deviation, or unilateral hearing loss.

37. HEAD IMPULSE, NYSTAGMUS, AND TEST OF SKEW (HINTS)
Fast phase that is unidirectional beating away from the affected side (peripheral)
Vertical or rotational (central)
Changes in direction (central)
2 – Patients with peripheral vertigo will have unidirectional, horizontal nystagmus, while patients with central vertigo can have rotatory or vertical nystagmus, or direction-changing horizontal nystagmus. 
In peripheral vertigo, it is common to have a horizontal-beating nystagmus with a fast phase that is unidirectional, beats away from the affected side, and increases in intensity when the patient looks in the direction of the fast phase. While vertical or rotational nystagmus reliably indicates an underlying central pathology, patients with central vertigo more typically have horizontal-beating nystagmus, mimicking peripheral vertigo. In such cases, the direction of the fast phase may change on eccentric gaze, i.e., the fast phase beats in one direction when looking to the right, and the opposite direction when looking to the left (or on returning to the midline). This direction-changing nystagmus reliably excludes a peripheral etiology.

38. HEAD IMPULSE, NYSTAGMUS, AND TEST OF SKEW (HINTS)
Alternate eye cover testing skew deviation
Focus on an object
Alternately cover each eye
As cover is moved eye will look up or down correcting for misalignment either up or down (Brainstem Stroke or central vertigo)
Patients with central pathology as a cause of vertigo will frequently have a right-left imbalance in otolith (gravity-sensing) function, resulting in a vertical misalignment of the eyes (i.e. one eye’s gaze slightly higher than the other). While focused on a fixed target, each eye is alternately covered. As the cover is moved from one eye to the other, the now uncovered eye must correct for the misalignment and will look up (or down) to focus back on the target. As the cover is moved back to the other eye, the newly uncovered eye will have to look down (or up) to correct its gaze back to the target. This slight correction is observed repeatedly as the cover is moved back and forth, from one eye to the other. Such ocular misalignment and skew deviation (with or without an associated head tilt and ocular fundus torsion) is frequently seen in patients with posterior fossa abnormalities (i.e. brainstem strokes). Alternate cover testing in patients with peripheral vertigo should result in no skew deviation or ocular tilt in the vast majority of cases.

39. HEAD IMPULSE, NYSTAGMUS, AND TEST OF SKEW (HINTS)
Must have continuous vertigo
Must be perfected (not an easy skill)
Not widely practiced in ED
Several points need to be considered when using the HINTS exam.  Most importantly, the exam should be performed only on patients with continuous vertigo.  In patients without active, continuous vertigo, the vestibulo-ocular reflex will remain intact and head impulse testing will be normal, with no corrective saccade observed.  This will be true in both patients with BPPV and in those without vertigo at all.  Such a finding is misleading, as it is considered indicative of a central pathology. This can lead to further unnecessary testing or hospital admission in such patients.
Before implementing the HINTS exam in one’s practice, the practitioner must exercise extreme caution. The HINTS exam has demonstrated excellent accuracy in distinguishing central from peripheral vertigo, but studies thus far have evaluated its use in the hands of neuro-ophthalmologists and neuro-otologists, whose familiarity with each component of the exam is likely to be much higher than the average emergency physician’s. In one study, neurologists tasked with performing the HINTS exam underwent a 4-hour tutorial prior to testing. Studies thus far have not evaluated the HINTS exam in the hands of the emergency physician, and additional training may be necessary before its routine use can be recommended.
Some may argue that the HINTS exam has limited utility in emergency department patients. Many feel that patients in whom stroke is considered should undergo MRI, or be admitted for further evaluation by a neurologist. However, the HINTS exam has been proven reliable when performed appropriately, and when negative should obviate the need for further testing in all but the highest-risk patients. Given the lack of objective findings in most patients with central vertigo, the HINTS exam will be a means of detecting central pathology in many patients who would otherwise be discharged home. Additionally, given the lack of sensitivity of MRI early in the course of posterior stroke, patients with a negative MRI but positive HINTS exam should still be admitted for further observation and testing. The key to the HINTS success will lie in appropriate training. Most emergency physicians are either entirely unaware of the HINTS exam, or are at least unfamiliar with its performance and interpretation. In such cases, a low threshold for imaging and neurologic consultation should remain in place. In an effort to improve patient care, emergency physicians should look to become adept at performing and interpreting the HINTS exam, and this tool should become a part of emergency medicine residency training.

40. Case study
76 YO male
Sudden onset of dizziness at 2300 (feeling off balance) unable to ambulate
HX of Bell’s Palsy with right facial droop, TIA, CABG, cardiac stents
No SOB, Nausea, vomiting, trouble with vision, trouble with hearing, no weakness, no numbness

41. Case study cont Neuro consult called Patient deemed to be having a CVA
CT negative
TPA administered
Only physical sign was lower extremity ataxia

42. Patient 2 September 41 Year old male Complains Denies
Spinning sensation (made worse with opening eyes and head turning)
Nausea
Vomiting
Denies
Headache , neck or back pain
CP, SOB, Palpitations

43. Patient 2 continued April 21
EMS called for vertigo (spinning feeling) with vomiting
Now has HX of Bells Palsey, migraines, vertigo, HTN
PERL + horizontal right sided nystagmus
Extremities intact with no motor deficits

44. Patient 2 continued ED differential DX Neurologist Dx
Benign positional vertigo, dehydration, doubt CVA, doubt posterior circulation ischemia
Neurologist Dx
41 YO male
Rotatory and horizontal nystagmus on lateral and upgaze
Gait ataxia
CT shows left inferior medial cerebellum stroke
Positive Romberg sign and widened stance
Negative deficits
Finger – to – nose intact

45. CASE STUDY
ALS and BLS dispatched for 41y/o male dizzy and vomiting. Upon BLS arrival PD on scene. PD stated they cancelled ALS prior to BLS arrival. Pt presents on knees vomiting into tub. Pt is alert and oriented to person, place and time. Pt is very diaphoretic and pale. Pt stated he began to not feel well two days ago. Pt stated it feels like vertigo. Pt had similar episode a year ago and took left over meclizine. Last night symptoms worsened and he was went to urgent care. This morning pt. began vomiting, nausea and feeling weak. Holding eyes closed is the only thing that helps dizziness. Pt stated he has been having a headache for past month. Vitals and PT moved to stair chair. Pt moved to stretcher and moved to ambulance. Pt vitals and monitored en route to hospital. Pt moved to room 3 and report and care given over to RN. 
P62 , rr 18, B/P
HX HTN takes Diovan

46. CASE STUDY
Patient 41 year old male comes to the emergency room with chief complaint of dizziness and vertigo symptoms since the past 2 days. Patient took meclizine from prior prescription. This morning with persistent dry heaving, dizziness, and diaphoresis. Patient called EMS because he was having severe vertigo symptoms of spinning. Patient acutely retching in the emergency room. Patient however believes that the dizziness is related to his BP which is now 129/90
Diff dx = Benign positional vertigo, dehydration, doubt CVA, doubt posterior ischemia

47. 1330 patient re-assessed not feeling any better headache has increased patient to be discharged with Compazine and valium and neuro consult
Patient CT was done which interestingly enough showed that patient has a indeterminate posterior cerebellar infarct. This appears to be acute based on clinical findings.
Patient admitted to hospital for neuro consult

48. NEUROLOGIST EXAM
A&O to norm; no acute distress: head normocephalic; no signs of trauma; no nuchal rigidity; full range of motion of the cervical spine; no edema of lower extremities
Cranial nerves: II. Visual fields full to confrontation; III, IV, VI extraocular movements intact with normal pupils, rotary and horizontal nystagmus on lateral and upgaze, worst on the left lateral gaze, no ptosis; V sensation on face intact in all three divisions; VII no facial asymmetry or weakness VIII hearing intact: xii tongue protrudes in the midline without atrophy or fasciculation's
Motor is normal.
Patient ultimately discharged with PT

49. QUESTIONS