Dementia

Neurological symptoms

DEMENTIA Loss of intellectual ability that interferes with a person's ability to function in their occupation or social situation.

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History When the difficulty start and how it progressed Evidence of ataxia and incontinence Hx of getting lost Hx of misuse of words Sloppiness in habits or dressing Hx of personality change Hx toxin exposure, alcohol or drug abuse Hx of trauma or headache

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Mental Status Exam 1. Check state of consciousness Not fully awake - suspect metabolic disorders or sol Delirium (not dementia) Clues: inattention, fluctuating Sx disturbance in sleep, prominent perceptual; abnormalities, increase autonomic activities 2. Check orientation 3. Check for aphasia 4. New memory Recall 3-4 unrelated objects in 5 min Can he remember money placed in his pocket? Knowledge of recent current events

• 5. Old memory • Info: on events occurring years ago (e.g. Martial Law or 1986 Edsa Revolt) • 6. Calculations • 7. Abstraction • How are a ball and orange alike? • How are Mitra and Santiago alike? • 8. Judgement • What would you do if a girl is drowning? • 9. Pictures - let him interpret a picture... • Does he focus on one tiny part? • Is he unable to integrate it (usual agnosia) • Can he draw or copy designs? • 10. Determine his mood and mental content • Is he sad or inappropriately cheerful? • Is he fearful or paranoid? • Is he active or pathetic, neat or sloppy? • Is affect labile?

Mental Status Testing What People May Be Asked To Do

What This Test  Indicates

State the current date and place, and Orientation to time, name specific people place, and person Repeat a short list of objects

Attention

Recall the short list of objects after 3 Immediate recall to 5 minutes Describe an event that happened in the last day or two

Recent memory

Describe events from the distant past

Remote memory

Interpret a proverb (such as "a rolling stone gathers no moss"), or explain a particular analogy (such as "why the brain is like a computer")

Abstract thinking

Describe feelings and opinions about the illness

Insight into illness

Name the last five presidents and the state capital

Fund of knowledge

Tell how they feel on this day and how they usually feel

Mood

Follow a simple command that involves Ability to follow three different body parts and requires simple commands distinguishing right from left (such as "put your right thumb over your left ear and stick out your tongue") Name simple objects and body parts, and read, write, and repeat certain phrases

Ability to use language

Identify small objects held in the hand and numbers written on the palm, and discriminate between being touched in one or two places (for example, on the palm and on the fingers)

Ability of the brain to process information from sense organs

Copy simple and complex structures (for example, using building blocks) or finger positions, and draw a clock, cube, or house

Ability to understand spatial relationships

Brush the teeth or take a match out of a box and strike it

Ability to perform an action

Perform simple arithmetic

Ability to solve math problems

• P.E. • 1. Gen. exam - look for liver, kidney, heart, lung or endocrine (thyroid) problems • 2. Focal signs e.g. field defect, aphasia • 3. Check pathologic reflexes ( Babinski, suck, grasp, shout) • 4. Test for smell • 5. Check BP or evident arrythmia

Treatable cause of Dementia • TUMORS • 1. If it presents silently as dementia it is often in the FRONTAL LOBE. • Frontal reflexes (suck, snout, grasp) maybe seen and slowness in carrying out tasks • Impaired smell • *Tumors in other areas show focal signs • 2. Tumors that obstruct the 3rd and 4th ventricle  hydrocephalus   dementia with few focal signs • 3. Memory difficulties or language problems are NOT common early features of tumors • 4. Dementia secondary to brain tumors pt usually presents within 6-12 months of onset of Sx

• NORMAL PRESSURE HYDROCEPHALUS (NPH) • 1. Check memory deficits, ataxia of gait and incontinence • Lower extremity spasticity and upgoing toes are common • *Demented person with normal gait does NOT have NPH • 2. Deterioration within 6-12 months is usual • 3. NPH following subarachnoid hemorrhage, meningitis or head trauma. Its etiology is OFTEN idiopathic

• SUBDURAL HEMATOMA • 1. Drowsiness in the elderly with recent personality changes, headache is usually presnt • 2. Mental changes seen over days, weeks or months • 3. Hx of head trauma may NOT be elicited • VIT. B12 DEFICIENCY • 1. Onset insidous over months to years • 2. Megaloblastic anemia usually present • * Blood smear, bone marrow and neuro exam except for dementia, maybe normal • * Folate deficiency may produce dementia • LIVER DISEASE • 1. Defect in memory, abstracting ability, attentiveness • 2. Note somnolence, generalized hyperreflexia, asterixis, myoclonus and hyperventilation • 3. Jaundice maybe ABSENT

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DEPRESSION -pseudodementia 1. Hx of previous psychiatric disease 2. Onset can be dated and Sx are brief 3. Pt complain of cognitive loss yet make little effort to perform simple tasks • They communicate strong sense of distress and give frequent `don't know` answers • 4. Other features of depression: • social withdrawal, anorexia, rumination of guilt, weight loss, insomnia episodes of crying

• Other Treatable Cause • Syphilis, fungal meningitis, toxins (metal), bromide poisoning, uremia, myxedema, Cushing's, thiamine deficiency, CO poisoning, CHF, drugs (barbiturates), chronic hypoxia, increase Ca, untreated hypertension, lung CA, SBE

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Nontreatable Cause 1. Alzheimer's Disease (Presenile Dementia) onset bet 50-65 yrs (> 65 yrs - Senile Dementia progression slow (yrs) look for memory problem, language difficulty, getting lost (-) nerological findings, pt neat and sociable Early disease _ Personality change Visual agnosia (ablity to see parts of but not recognize object) 2. Atherosclerosis (Multiple Strokes) bilateral pyramidal signs (upgoing toes) Hx of suggestive of small focal lesions Pseudo Bulbar Signs - emotional lability (easy crying) increase jaw jerk and gag, dysathria, dysphagia NSAD Tx of HPN

• Benefits of having Alzheimer's disease • 5. You never have to watch reruns on television. 4. You are always meeting new people. 3. You don't have to remember the whines and complaints of your spouse. 2. You can hide your own Easter eggs. 1. Mysteries are always interesting.

• CREUTZ (?) FELDT-JACOB DISEASE • dementia + upper motor neuro signs, myoclonus, basal ganglia signs, startle to noise and Bright Lights • death occur in months • HUNTINGTONGS CHOREA • Dementia, personality and emotional disorder precede chorea • FxHx - autosomal dominant

Love is not "it's your fault", but "I'm sorry", not "where are you?", but "I'm here", not "how could you?", but "I understand", not "I wish you were here", but "I'm thankful you are".

HEADACHE

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HISTORY A. Character of Headache Pain Migraine - periodic, throbbing, severe, frequently unilateral, often over the eye. - associated with Photophobia, sensitivity to sound, nausea or vomiting. Tension - tend to be diffuse, steady, occipital or frontal and "bandlike". Cluster - very painful, knifelike, unilateral and over the eyes.

• How long has the headache been present ? • • Migraine • - starts at teenage years, decreases during 30's and 40's; exacerbated or relieved during menstruation, pregnancy or around menopause. • (+) FH of migraine. • (+) History of motion sickness as a child. • Tension • - seen after age 10. • prominent in times of stress and at end of the day. • do not occur in cyclic pattern. • Cluster • - seen in Patients 20-60 y.o. • HA comes in clusters, last weeks to months and then subside. • males > females.

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Prodromes Classic Migraine preceded by visual or other prodome e.g. flashing lights, blind spots, hemianopsia, difficulty in talking, tingling face or extremity to hemiparesis (hemiplegic migraine), sensory symptom that spread slowly along that spread slowly along an ext. (“marching symptom). positive then negative symptom e.g. flashing light ⇒ darkness / tingling – numbness-scalp tenderness. Common Migraine - no prodrome Cluster - eye tearing , facial flushing or runny nose (alitonic phenomena) ipsilateral to headache. When do headaches occur? Migraine occur any time (maybe awaken during sleep). maybe associated with menstruation, hunger, alcohol ingestion, chocolates, high altitude. exacerbated by contraceptive pills , hyperlipidemia, HPN Tension - appear at the end of the day.

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Cluster occur at the same time everyday. HA is strong enough to awaken the patient maybe precipitated by alcohol intake. Factors that makes Headache better or worse Migraine once established, relieved by sleep and often improved by vomiting. • Sleep has NO effect on cluster headache • Tension • relieved by relaxation and massage of the back of the neck.

• Headache of Tumors • worse with coughing or straining (as migraine), worst on arising in the morning. • Does medication affect the head-ache? • Migraine • Ergot if given early , prevents or alleviates headache. • Tension • respond to Aspirin or parace-tamol. • Cluster • not relieved by any medications once there is headache. • How long does the Pain last ? • Migraine - Hours to a full day, sometimes longer. • Tension - Hours to days. • Cluster - minutes to hours.

• On tension headache • Seen after age 10 bec there is no error of refraction yet • Cause: stiffness of frontooccipitalis muscle, eye problem ,colds, fever, tension • Treatment: tilt head and gaze upward , Biogesic, NSAIDs • On cluster headache • Continuous, most painful, “your best excuse for absenting yourself” • DDx: glaucoma which usually presents with photophobia

• Is depression a factor? • Depression and anxiety is important • Determine patient’s lifestyle, personality, etc for patients with daily headache for a long time • Determine adjustment to school, job, illness at home, etc.

• Examination of Patients • Look for focal signs indicative of structural lesions ( see fundi, look for papilledema) • Check for autonomic dysfunction (cluster)-miotic pupils, ptosis, red eye, unilateral nasal congestion • Note sweaty hand and feet or scalp tenderness (migraine) • Development of stiff neck during the “worst headache of my life” (subarachnoid hemorrhage) • Migraine attacks occurring on the same side, suspect AVM, look for bruit, migraine occurring on either sign is usually benign

• Headache over the eye in elderly (5070y) maybe due to temporal arteritis • -tender temporal artery, elevated ESR, may lead to blindness if not treated early • HPN may exacerbate migraine esp if labile • Glaucoma- elderly, headache, eye pain, vomiting, eye redness, palpate globe

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Headache features suggestive of a spaceoccupying lesion Subacute and progressive in nature New onset in adult life (>40 yr of age) or significant change in established pattern Association with any of the following: Nausea or vomiting not explained by migraine or systemic illness Nocturnal occurrence or morning awakening Precipitation or worsening by changes in posture Confusion, seizures, or weakness Any abnormal neurologic sign

• Brain tumor •

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Headache is present in about 60% of patients with brain tumor and is the predominant complaint in half of these patients. However, it is the exception when a patient with headache alone harbors a space-occupying lesion. More commonly, seizures, weakness, and subtle cognitive changes are present, and these should raise red flags. Traditional features of brain tumor (eg, vomiting, papilledema, and headache that is worse in the morning or worsened by Valsalva's maneuver) are present in a minority of patients and cannot be relied upon to raise the index of suspicion. As a general rule, headaches due to space-occupying lesions have poor localizing value except when they are unilateral. They are usually frontotemporal and may be mistakingly diagnosed as tension or "sinus" headaches. Headaches caused by brain tumor are new or different and are usually subacute and progressive, moderate to severe in intensity, and resistant to relief by use of analgesics.

• Subdural hematoma

Headache is the single most common symptom of subdural hematoma; it is often bitemporal or generalized. Subdural hematoma is more common in elderly patients but may go unrecognized because cerebral atrophy allows the development of a larger hematoma before pain-sensitive intracranial structures are compromised. Chronic subdural hematoma may give rise to indolent chronic headache without obvious neurologic signs or symptoms for a prolonged period of time. Because only 60% to 70% of patients with subdural hematoma have a history of antecedent trauma, an attempt to elicit the following features is important and should lead to neuroimaging: • Changes in personality or cognitive abilities • Focal and sometimes intermittent weakness, seizures, or sensory changes • Excessive sleepiness, lethargy, or decreasing level of consciousness

Intraparenchymal hemorrhage Headache accompanying intraparenchymal hemorrhage is severe, invariably acute or subacute in onset, and often associated with obvious focal hemispheric or cerebellar signs, nausea, vomiting, and impaired consciousness. The presence of brain-stem symptoms or signs, ataxia, or vomiting should suggest a cerebellar hemorrhage, which is a neurosurgical emergency. Patients can rapidly deteriorate and succumb from acute hydrocephalus because the hematoma obstructs the egress of CSF from a compact posterior fossa.

Nonstructural causes The nonstructural causes of headache can be subdivided according to the painsensitive cephalic structure affected, namely, the intracranial and extracranial blood vessels and the dura mater.

• Vascular disorders Important disorders of the blood vessels that cause headache include subarachnoid hemorrhage, cerebral ischemia, arterial dissection, various vasculitides, and cerebral venous thrombosis.

Subarachnoid hemorrhage: A severe, unusual, and unrelenting headache of abrupt onset should always prompt a thorough diagnostic search for a ruptured intracranial aneurysm or arteriovenous malformation. Nausea and vomiting, nuchal rigidity, photophobia, and decreased level of consciousness always cause alarm, but the subtle "warning leak" headaches that precede about 50% of subarachnoid hemorrhages unfortunately may go unrecognized . These headaches must be identified to preempt imminent catastrophe. The following clues can help in detecting the deceptive small hemorrhage: • Unusually severe and abrupt hemifacial pain (caused by aneurysmal distention or subarachnoid blood irritating the trigeminal nerve) • Onset of headache with exercise or intercourse • Spread of pain to neck, interscapular region, or low back • Fever • Slight alteration of awareness • Subtle meningeal irritation (resistance to passive flexion of neck) • Visual blurring, diplopia, or "soft" neurologic signs (ie, asymmetry in pupillary response, equivocal extensor plantar response, pronator drift)

Cerebral ischemia: • Although not commonly recognized, headache occurs in about one third of patients with cerebral infarctions and in 10% to 15% of those with transient ischemic attacks. • Moreover, a "sentinel headache" may be a premonitory symptom of thrombotic or cardioembolic stroke in up to one third of cases. • The headaches may occur hours to weeks before the ischemic event, which underscores the importance of recognizing them as harbingers of stroke.

• In contrast to the headaches of hemorrhagic stroke, those of ischemic cerebrovascular disease vary in severity, quality, and duration and often resemble tension or migraine headaches. • Although localization does not reliably indicate the vascular territory involved, hemicranial headaches are likely to be ipsilateral to the ischemic hemisphere. • Headaches occur more often with large-vessel occlusive disease (25% to 32%) than with small-vessel lacunar infarctions (15% to 23%) • are more often associated with ischemia of the posterior circulation, and are more common in patients with a previous history of headache. • The possibility of ischemia must be carefully considered in a middle-aged or older patient with vascular risk factors who presents with a new and unexplained headache.

Arterial dissection: • Arterial dissection accounts for up to 20% of strokes in young adults. • Cephalic pain is an extremely important symptom in patients with carotid or vertebral dissection, because it is often the inaugural and sometimes the only symptom. • Headache is usually of sudden onset and may precede retinal or hemispheric ischemic symptoms by hours to weeks.

• Carotid dissection is more common than vertebral dissection. The latter, which may begin as acute neck pain or occipital headache, often goes unrecognized until ischemic symptoms occur, but carotid dissection is frequently accompanied by clinical clues that should invoke suspicion (table 2). • If these are recognized early, appropriate investigations and anticoagulant treatment may prevent an imminent cerebral infarction.

Table 2. Clues to carotid dissection  Onset temporally related to cervical manipulation, sustained exertion, or trauma  Sudden unilateral neck pain or headache with radiation to ipsilateral face, eye, or ear  Horner's syndrome without anhidrosis  Amaurosis fugax  Pulsatile tinnitus  Ipsilateral tongue weakness (hypoglossal nerve palsy) and dysgeusia  Cervical bruit or tenderness  Diplopia  Syncope

• Vasculitides: Inflammation of dural, intracranial, or extracranial blood vessels causes headache. The vasculitides of major importance with respect to headache include the following: • 1. Temporal arteritis. This is an important cause of headache in late middle-aged and older adults. When left untreated, it often leads to permanent blindness. Headache is a major feature in more than 90% of cases. Because of the variability in presentation, attention to the following features helps raise the index of suspicion: • Age greater than 50 years • New-onset, localized, progressive headache • Local symptoms (superficial temporal artery swelling, tenderness, and pulselessness)

• Cranial symptoms (transient visual obscurations, diplopia, mental sluggishness and, rarely, stroke) • Systemic symptoms (fever, weight loss, anorexia, malaise, myalgias, sweating, and chills) • Systemic markers of inflammation • An elevated erythrocyte sedimentation rate (>50 mm/hr) • Elevated levels of acute phase reactants (Creactive protein, von Willebrand's factor, fibrinogen, platelets, lymphocytes, immunoglobulins)

• 2. Systemic vasculitides. These include polyarteritis nodosa, systemic lupus erythematosus, and Wegener's granulomatosis. They may present with headache as a major but often undefining feature. Focal neurologic signs and symptoms, seizures, behavioral and cognitive dysfunction, and arterial stroke occur in conjunction with other evidence of systemic or visceral organ involvement (6).

• 3. Isolated central nervous system vasculitis. This noninfectious recurrent angiopathy is confined to the central nervous system. It presents with severe headache in addition to focal or global neurologic symptoms and signs. As is the case with systemic vasculitides, MRI often reveals evidence of significant subcortical white matter involvement even when a CT scan is normal. Constitutional symptoms are usually absent and there are no systemic markers of inflammation or visceral organ involvement. Angiography and CSF analysis give abnormal results in most cases but, like MRI findings, they are nonspecific. Therefore, a tissue diagnosis (brain biopsy) is required, using diagnostic criteria established by leading authorities in this field (7). The outcome is invariably fatal if the condition is left untreated, but immunosuppressive therapy is often lifesaving.

• Cerebral venous thrombosis: Intracranial venous occlusive disease is notoriously difficult to recognize. (Symptoms are often nonspecific and CT imaging is frequently unrevealing). Despite the variety of presentations and causes, headache is the most common symptom (75%) and often the initial one. The headache may mimic that of subarachnoid hemorrhage, migraine with or without aura or, more commonly, benign intracranial hypertension. The headache may also occur in isolation, and the diagnosis may be suggested only because of predisposing underlying conditions (table 3). Because the headache has no typical clinical characteristic or specific temporal profile, attention to associated symptoms, which are present in more than 95% of cases, raises intracranial venous occlusion as a diagnostic possibility.

• Table 3. Most common causes of intracranial venous thrombosis • Infections (otitis media, meningitis, sinusitis) • Pregnancy and changes during postpartum period • Oral contraceptive use • Underlying malignant process • Connective tissue disease, especially Behçet's syndrome • Hypercoagulable disorders • Antithrombin III deficiency • Protein C deficiency • Protein S deficiency • Dysfibrinogenemia • Paroxysmal nocturnal hemoglobinuria • Activated protein C resistance • Inflammatory bowel disease

Most commonly, papilledema, focal motor or sensory deficits, seizures, or drowsiness and confusion accompany the headache of cerebral venous thrombosis and should suggest the disorder, particularly when the CT scan is negative.

Meningeal headaches Headache is often the presenting, most prominent, and sometimes only symptom of conditions that primarily involve the leptomeninges.

Infectious meningitis: • • •

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This is usually the first diagnostic consideration in a patient with headache and fever. However, fever alone, distant infection, and infection of adjacent structures are also frequent causes of headache, and astute clinical judgment is a necessity. Careful attention to important associated signs is critical, especially in elderly, young, comatose, and immunocompromised patients; the diagnosis can be subtle in early stages of infection, particularly in these special groups. In the absence of focal neurologic signs, an immediate lumbar puncture is essential when the following features are present: Acute or subacute headache with fever (including low-grade) Meningism (even a slight limitation of passive forward neck flexion) Lethargy, altered awareness or behavior Photophobia, irritability, myalgia, anorexia, vomiting Signs of systemic infection (cough, coryza, skin rash, leukocytosis, elevated erythrocyte sedimentation rate)

Encephalitis: • Generalized headache of rapid onset, particularly if associated with fever, confusion, altered level of consciousness (delirium to coma), meningism, focal neurologic signs, or seizures, should alert the physician to the possibility of encephalitis. Encephalitis is treatable when due to herpes simplex virus, Coxiella burnetii, and Listeria monocytogenes. • Encephalitis caused by herpes simplex virus is usually an acute fulminant infection with a high mortality rate if unrecognized. Occasionally, there may be a prodrome of less severe headache accompanied by myalgia, fatigue, and fever that precedes the cataclysmic event by days. Even more rare is a headache that progresses over months and is associated with chronic encephalopathy. • MRI is the imaging procedure of choice. Typically, T2signal abnormality is seen in the medial temporal lobes.

Summary • Headache can be an invaluable premonitory signal of imminent subarachnoid hemorrhage and cerebral infarction and can herald the onset of ominous and sometimes elusive disorders (arterial dissection, encephalitis, systemic and central vasculitides, and cerebral venous thrombosis) which have the potential for neurologic catastrophe and are often not obvious on routine CT brain imaging. • Only rarely does serious underlying disease give rise to a headache that exactly mimics a migraine or tension headache. Inevitably, there are atypical features or warning signals. • A limited number of serious causes for headache which may be "CT-negative" should be considered in patients with "red flag" manifestations, such as seizures and cognitive changes. These should prompt further investigation with MRI and/or lumbar puncture.

DIZZINESS • DIZZINESS • VERTIGO • illusory sensation of turning or spinning (either of Pt. or sur-rounding). • DIZZINESS • ill-defined; lightheadedness, gid-diness, feeling of uneasiness in the head. • Determine if : • Peripheral - (labyrinth, vestibular or cochlear). • Central - (brainstem, cerebellum or cerebral cortex). • Systemic - ( CV , metabolic).

Peripheral

Central

Latency

3 – 10 sec.

none

Duration Fatigability N/V

40 sec. Yes Usually Present

> 40 sec. NO Not prominent / Absent

Vertigo

= to nystagmus

not prominent

Vertical nystagmus Rotary nystagmus

Negative

Maybe present

Usually seen in Seldom present peripheral lesion

HISTORY • Determine if the paroxysmal or related to head position. • Associated nausea, vomiting, headache. • Symptoms of diplopia, dysarthria, numbness. • Tinnitus, deafness. • Lapse of awareness. • EXAMINATION • Examine CVS. • Ear canal and hearing (watch tick, spoken voice, finger rubbing {different frequency}).

• Neurol Exam - emphasis on CN, cerebellar, nystagmus (horizontal or vertical). • Check for positional vertigo and nystagmus • from sitting to supine while quickly turning head to the side. • note nystagmus, latency of response, associated vertigo, fatigability. 5. Caloric Testing • minimal icewater CT. • Pt. lies supine with head eleva-ted 30 °. • irrigate each ear with 0.2 cc icewater. • *Nystagnus ( fast component ) is in the direction of opposite ear and should last 1 minute • note the symmetry of response to each ear (do formal Caloric Test for confirmation).

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Determine if lesion is Peripheral or Central Peripheral Lesion associated with deafness or tinnitus (8th NN dysfunction). Pt. reports caloric testing repro-duces dizziness or a unilateral ↓ caloric response. no central signs. Central lesion S/Sx - e.g. Cerebellar ataxia, CN abnormality, diplopia, dysarthria, papilledema. nystagmus is marked with little or no vertigo, vertigo parallels nystagmus if Peripheral. Nystagmus prominent looking at side of the lesion; the fast component changes with look-ing at the different directions. Acute labyrinthine or Vestibular disorder nystagmus prominent when looking at Normal ear. Peripheral patient fall to the side of lesion and away from fast comp. of nystagmus. Central ( e.g. cerebellar infarct) Pt. fall to the side of lesion {i.e. toward the fast comp. of nystagmus}. Determine if lesion is Peripheral or Central

• PERIPHERAL LESIONS • Middle ear disease involving the labyrinthine Check for otitis and abnor-mallities of Tm? ototoxic drugs. excessive earwax can cause dizziness. • MENIERE'S DISEASE vertigo, tinnitus and deaf-ness. Tinnitus and stuffiness ⇒ violent attack of N / V, sweating, ↓ hearing. nystagmus present during attacks only. occur between 30-60 years old, paroxysmal, acc. by residual tinnitus and hearing loss after several attacks. vertigo last 1-2 hours.

• Benign Paroxysmal Vertigo or Episodic Vertigo ppted. by turning head or change in position. no hearing loss, N calorics, self- limiting. • Acute Labyrinthitis etiology : Bacterial or Viral. sudden onset with severe vertigo and GI symptoms. last 1-3 days. usually with spontaneous nystagmus toward good ear, hearing may or may not be affected. N calorics. • Vestibular neuronitis sudden vertigo and nausea w/out auditory S /Sx. caloric test with ↓ function on affected side. • Post - traumatic Vertigo prob. 2° to labyrinthe damage. Sx of peripheral vestibulo-pathy.

LESIONS WHICH BEGIN PERI-PHERALLY THEN SPREAD CEN-TRALLY • ACOUSTIC NEUROMA Early Sx - tinnitus, ↓ hearing, dizziness or disequilibrium. Later - CN dysfunction (↓ corneal reflex, facial weakness) and cerebellar signs. • CENTRAL LESIONS • Posterior Fossa Tumors check cerebellar and other brainstem signs. look for evidence of ICP (fundi). • Vascular Lesion (Vertebrobasilar Insufficiency) brainstem Sx (diplopia, slurred speech, numbness, trouble swallowing). CN dysfunction, motor or sensory loss.

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CENTRAL LESIONS Posterior Fossa Tumors check cerebellar and other brainstem signs. look for evidence of ICP (fundi). • Vascular Lesion (Vertebrobasilar Insufficiency) brainstem Sx (diplopia, slurred speech, numbness, trouble swallowing). CN dysfunction, motor or sensory loss.

Points to Remember : • • • • • • •

Dizziness and vertigo as first sign later (within months). Followed by Sx of brainstem dysfunction. Lateral medullary syn-drome may begin with vertigo. Cerebellar hemmorhage or infarct may initially mani-fest with acute dizziness, vomiting, inability to walk or stand and severe head-ache. Patients with subclavian steal syndrome may have attacks of vertigo. Dizziness + 8th NN dys-function probably NOT vascular. Vertigo is seldom seen in Carotid Artery disease.

Temporal Lobe Epilepsy • causes vertigo. • history of staring spells, auto-matism, de javu phenomenon, abdominal pain. Dizziness after Head Trauma • nonspecific. • benign paroxysmal vertigo. • Posttraumatic epilepsy. Basilar Migraine • Vertigo + Basilar A. Sx • Vertigo ,visual disturbance (e.g. Scotoma ) , tinnitus , blackouts ---- throbbing occ. headache after Sx subsides. • Check for diplopia.

• SYSTEMIC LESIONS • Arrythmias ∀ ↓ OR ↑ BP ∀ ↓Blood Sugar • CHF • Anemias • Thyroid Disease • Drugs- Ototoxic, Hypotensive • Patients with Multiple Sensory deficits (Elderly) may have Dizziness. • Dizziness or Vertigo with no apparent cause. • Psychogenic- 2° to Hyperventilation Most common cause of Dizziness.

END OF LECTURE