HEADACHE: Red flags: 1st or worst headache Headache frequency and severity increasing Increasing frequency of vomiting and

headache on walking Headache triggered by cough/straining/posture Persistent signs and symptoms after attack Meningeal or cortical signs, encephalotis Trauma Meningitis: Fever, neck stiffness, vomiting. SOL: Mood/behavioural changes, vomiting without nausea, cortical signs, hxx of Ca. with HA (metastasis), night sweats, loss of weight, night pain, changes special senses. Haemorrhage: Trauma, acute onset of HA, anticoagulants, changes in behaviour. Classification: Primary HA: Migraine, tension type, cluster and cervicogenic (referred from the ears, eyes, nasal passage, teeth, sinuses, facial bones and csp via CN V, VII, IX X and upper three cervical roots. Secondary HA: Brain tumour, infections of the brain parenchyma or meninges, haemorrhage

Questions: Age of onset Presence or absence of an aura an prodrome Mode of onset: acute, subacute, chronic, or recurrent and episodic o Acute onset: It should always raise the suspicion of subarachnoid haemorrhage, dissection of basilar/carotid artery or a haemorrhagic stroke. o Subacute onset and progressive HA: It includes most most of the serious cause of HA o WORRYING THINGS: ACUTE/SUBACUTE ONSET, INCREASING SEVERITY OF HA, PERSISTENT ASSOCIATED NEUROLOGICAL SYMPTOMS OR SIGNS, A DETERIORATION OF CONCIOUSNESS LEVEL, SEIZURES, ASSOCIATED FEVER OR LOCAL TENDERNESS (TEMPORAL ARTERY) Subsequent course: episodic, progressive or chronic o Recurrent and episodic: Recurrent and episodic is usually bening and is very rarely due to sinister pathology. The most common cause are migraine, tension type HA and trigeminal autonomic (cluster). o Chronic daily HA: Chronic daily HA is a descriptive term that is characterised by HA occurring > 15 days per month. The most common cause is chronic migraine, which is complicated by medication overuse HA.

New daily persistent HA: Hxx of HA in almost all days from the start of the initial presentation. Most common cause: migraine and tension type HA. But, possible secondary cause: subarachnoid haemorrhage, low/high csf pressure HA, chronic meningitis and post-traumatic. This presentation should prompt to further investigation and rule out secondary causes oh HA. Site: unilateral or bilateral; frontal, temporal or occipital; radiation to neck, arm and shoulder (cervicognic) Character of pain: constant, throbbing (migraine), stabbing, dull ache, pressure like, tight band (tension-type) Frequency and duration: constant or intermittent with pain lasting seconds, hours or days Accompanying features: neck stiffness (meningitis), autonomic symptoms (cluster) and aura like symptoms (visual, motor, sensory or speech)(migraine) Exacerbating factors: movement, light, noise, smell, coughing, sneezing or bending (SOL) Precipitating factors: alcohol (cluster HA), menstruation (migraine), stress (all HA types), postural changes (high or low CSF volumes), trauma (subdural haemorrhage or post-traumatic migraine) Particular time of onset: mornings (raised intracranial pressure) or awaken at night (cluster HA) Past hxx of HA and response to any type of ttt Family hxx: migraine or intracranial haemorrhage General Health: systemic ill health, existing medical conditions, overweight, depression, low mood, stress Drug hxx: analgesic overuse, the oral contraceptive pill, recreational drugs, anticoagulants, vasodilators. COMMON CAUSE OF RECURRENT EPISODIC HA: CAUSE CLINICAL FEATURES Migraine -HA attack lasting 4 to 72 hours -TCS: vc and vd -Unilateral -Pulsating/throbbing quality - Subacute onset -Moderate to severe intensity Accompanied by: nausea/vomiting, phono/photophobia, Triggered by: Exercise, strong smells, bright light, loud sounds, tiredness, fatigue, menstruation -Not attributed to another disorder -At least 5 attacks fulfilling this criteria Cluster -Severe HA -Young men -Unilateral retro/periorbital +temporal pain -Acute onsent reaching crescendo within minutes -Associated autonomic features: conjuctival lacrimation, ptosis, miosis, nasal congestion/rhinorrhea, facial flushing/sweating/pallor, associated restlessness/agitation

Tensiontype HA

Cervicog enic HA

-Attacks last 15-180 minutes -They can occur up to 10 times per day -May have circadian periodicity (awaken at night) -Triggered by alchohol -Bilateral location -Tight band around the head or a pressure like sensation (non-pulsating quality) -TCS: Muscular tension (sucoccpitals and trapezious) -Mild to moderate severity -Waxes and waves lasting variable amounts (30 minutes to 7 days) -Featureless: no vomiting/nausea, no photo/phono -Neck involvement -Decreased ROM of the csp -TCS: (C1-C3) greater occipital nerve, greater auricular nerve: Refer pain -Ipsilateral neck, shoulder and arm pain -Unilateral HA without side shift -Moderate to severe, no throbbing, starting in the neck -Nausea -Photo/phono -Dizziness -Blurred vision -Difficulties swallowing -Ipsilateral oedema, usually in the periocular area Ttt: C1-C2: sympathetic distribution: influencing the vc/vd

SUBACUTE-ONSET HA: Intracran Features associated with increased intracranial pressure: HA exacerbated eal by coughing, sneezing, bending over or straining; blurring of vision on tumour bending forward; papilloedema; nausea/vomiting Associated neurological signs and symptoms Meningiti Fever, neck stiffness, +ve knernigs sign s Giant cell -Over 50 arteritis -Visual disturbances: acute monocular loss of vision -Jaw claudication -Associated PMR -Elevated ESR and CRP -Tender thickened superficial temporal artery + absent pulsation Acute Pain typically frontal, orbital or ocular, accompanied by persistent visual glaucoma impairment, fixed oval pupil and conjuctival injection Subdural -Hxx of head injury haemorr -Elderly/alcoholism/anticoagulants hage -Bridging veins parietal lobe -Fluctuating level of consciousness, confusion, focal neurological signs Low CSF Orthostatic HA following lumbar puncture or a spontaneous or traumatic volume chronic lekeage of CSF PostMost common is migraine traumatic HA

Common causes of acute onset HA Subarachnoid haemorrhage -Explosive and instantaneous -Thunderclap HA -Circle of Willis aneurysm into CSF -Young, exertion -Meningism -Hit with a brick -Worst HA Haemorrhagic stroke -Hxx of hypertension, smoking, diabetes, anticoagulation -Focal neurological signs depending on the site of bleed Migraine Vertebro-basilar ischaemia

HEARING LOSS AND TINNITUS: Def. Tinnitus: is the sensation of ringing, buzzing, hissing, chirping or whistling in the ear. It is a manifestation of disease of the middle ear, inner ear or cochlear component of CN VIII, and is usually accompanied by some degree of deafness. Sensoryneural deafness accompanied with high pitch, conductive: low pitch. It can be intermittent/continuous, unilateral/bilateral, high pitch/low pitch. Causes of deafness and tinnitus: Site of damage Cause Outer ear Was, foreign body Middle ear Trauma (# temporal bone), infection (otitis media), otosclerosis Cochlea Age, infection, noise induced, drugs (aminoglycosides), Menieres disease th 8 CN Lesion cerebellopontine angle, acoustic neuroma, basal meningitis, malignant infiltration Brainsteam (rare) MS, neoplasm, infarction Cerebral hemisphere (rare) B lesion temporal lobes (infarction, neoplasm) Pts complaining from tinnitus: Anaemia, fever, hypertension, Pagets disease, hyperthyroid, loud sounds, head trauma, antibiotic use or drug (aspirin, serotonin, quinidine, benzodiazepines withdrawal) and alcohol misuse occasionally complain of tinnitus. Pulsatile tinnitus (rarely life threatening condition): arteriovenous malformation, carotid stenosis, artherosclerosis, bening intracranial hypertension, Giant Cell Arteritis, jugular bulb turbulence Just when all the underlying conditions have been excluded can the pt be considered to have idiopathic tinnitus Q: -Onset: Trauma, infection,

-Unilateral/Bilateral: Unilateral further investigation because it could be early presenting feature of CN VIII tumour and it is not necessarily accompanied by hearing loss or vertigo. (MRI in the cerebellopontine angle) -Constant/intermittent -Any hearing loss -Low pitch: /High Pitch -Objective character: Pulsatile (arteria), muscular contraction -Associated with any other systemic condition -Bruxism: Can change the quality of tinnitus Examination: Ears, nervous system, neck and audiometry DIZZINESS AND VERTIGO:

CAUSES OF VERTIGO: 93% = BPV, vestibular neuronitis or Menieres PERIPHERAL Often with nausea/ vomiting and positive Dix Hallpike manoeuvre (which shows fatiguability) Often rotatory vertigo Nystagmus usually horizontal rotational. Disappears on focussing gaze. Usually clear provocation and a latent period after e.g. head movement Episode of short duration Often worse am, often agg by certain positions Sudden/ obvious onset Tullios sign- nystagmus + vertigo triggered by certain frequencies/ loud noises Often with hearing loss Balance only slightly impaired Peripheral vestibulopathy Inflammation of the vestibular nerve usually caused by viral infection (upper resp Vestibular tract infection). neuronitis Duration: 2-3 weeks Single or recurrent sudden episodes of true vertigo lasting from hours to days and often. Associated initially with vomiting. Vertigo may be provoked by head movement, but not necessarily by a particular head position. Incidence: Young- middle age adults Vertigo episodes last a few secs in late stages. No hearing loss or tinnitus, main symptoms id VERTIGO. Sometimes nystagmus labyrinthitis Acute labyrinthitis Inflammation of the labyrinthine organs (cochlea and vestibular system) caused by viral or bacterial infection. Agg by changes in head position Incidence: 30-60. Symptoms: Vertigo, dizziness, loss of balance and hearing loss. When the condition is associated with hearing loss, the entire labyrinth is assumed to be involved, and the term labyrinthitis is used. Acute/ recurrent May be triggered by a virus. peripheral PPW variable disturbance from sudden severe vertigo, nausea, and vomiting vestibulopathy without any hearing disturbance or facial weakness to only a sensation of lightheadedness or floating, or a feeling of "walking on tennis balls.". The acute symptoms usually resolve in a few days to a week, but may recur in weeks or months. Cholesteatoma Cyst-like lesion filled with keratin debris, most often involving the middle ear and mastoid, progressive conductive unilateral hearing loss Otitic Herpes zoster Vesicular eruption affecting the ear; caused by reactivation of the varicella-zoster virus An infection characterized by pain in the ear, followed in 1 to 10 days by a vesicular eruption in the external ear. When the VIII and VII nerves are affected, there is a combination of facial weakness, hearing loss, and vertigo (RH syndrome)

Perilymphatic fistula

Benign positional vertigo / nystagmus

Breach between middle and inner ear often caused by trauma or excessive straining/ valsalva or scuba diving. Pushing on tragus and ext. auditory meatus may trigger vertio/ nystagmus (Henneberts sign). Valsalva also may trigger it. Vertigo episodes last a few secs-1 hour, hearing loss Cause: dislocation of particulate material from the otoliths into the post semicircular canals. Incidence: middle-age and older patients (55yo); 2 women: 1 men Agg: by changes in head position(particularly lying down, bending forward) Common causes: head trauma (17%) and viral neurolabyrinthitis (15%), age/ idiopathic which dislocates Ca2+ carbonate crystals (otoliths) and alters their position on hair cells or into canals s/ signs- transient and episodic vertigo rarely lasting longer than 40 seconds. Usually occur with a certain position e.. lying down/ turning. Often rotatory vertigo which is worse am. s should be reproduced by pro vocative manoeuvres eg Hallpikes with a delay (latency) before onset of s
Pt quickly moved from sitting to horizontal with head off plinth and turned to 45o. Observe for nystagmus. Repeat with head to other side/ not turned.

Post-traumatic vertigo

Drugs

Meniere's syndrome

ttt. Certain exercises/ head manoeuvres may move the otoliths Following head trauma- need to exclude other CNS damage. s may appear days/ weeks after trauma Mechanism: heamorrage/ otolith redistribution. s similar to benign positional vertigo/ peripheral vertigo Ttt. Exx or if not resolving nerve sergury. Prognosis: good, weeks- months Aminoglycosides and quinines Recurrent episodes of vertigo, hearing loss, tinnitus, or aural Cause: fullness caused by increased volume of endolymph in the semicircular canals and degeneration of the organ of Corti Incidence: 30-50 yoa > s severe vertigo, tinnitus, fluctuating hearing loss and ill-described aural sensations of fullness with spontaneous recovery in hours to days. Initially, the patient develops a sensation of fullness and pressure along with decreased hearing and tinnitus in a single ear. No consistenat provoking factors. This is followed by severe vertigo, which reaches peak intensity within minutes and slowly subsides over hours, the Pt may fall over. There is persistent sense of disequilibration for days after an acute episode Causes: vol of endolymphatic fluid=> distension of canals due to bacterial, viral, and syphilitic infections or idiopathic. Prognosis: not good, may become bilateral, hearing loss common, generally attacks in frequency.

Vertigo episodes last a few secs in late stages but in initial stages may last for hours
acute otitis media chronic ear infection hereditary degenerative disorders of the end organ local tumors Local ischamia Painful

otosclerosis Head trauma Type 2 neurofibromatosis

e.g. invasive disease of temporal bone= painful Vertebrobasilar transient ischemic attack (TIA) or focal ischemic stroke of the end organ, particularly in an elderly patient. Check other CNs Hardening or thickening of the tympanic membrane caused by age or recurrent infections of the ear. Progressive conductive hearing loss => bilateral acoustic neuroma

CENTRAL Central pathological causes of vertigo result from dysfunction of the vestibular portion of the VIII nerve, the vestibular nuclei within the brainstem and their central connections. Nystagmus usually purely horizontal/ vertical or rotational. Rarely on fixing gaze. Long duration little or no latency and no fatiguability Insidious onset (except when due to acute CVS cause Other neurological signs Nausea and vomiting tends to be less severe More severe instability and walking problems Brainstem Ischemia and Infarction vertebrobasilar The posterior circulation supplies blood to the brainstem, cerebellum, peripheral insufficiency vestibular apparatus, in addition to other structures s transient clumsiness, weakness, loss of vision, diplopia, perioral numbness, ataxia, drop attack, and dysarthria (May just be dizziness) Signs- weakness, clumsiness, or paralysis. Crossed signs (1 half of head, other half of body), possibly transient visual loss. Ataxia, imbalance, unsteadiness, or disequilibrium if labyrinth/ cerebellum affected brainstem TIAs should be accompanied by neurologic symptoms or signs, in addition to vertigo or dizziness. (Dizzyness not always present) vertigo lasts mins- 1hour Stroke Internal auditory Infarction in distribution => Sudden hearing loss with moderate dizziness artery blockage Causes: vasculitis e.g. syphilis, SLE or PAN Brainstem infarction May affect atherosclerotic Pts nystagmus, hyperreflexia, internuclear ophthalmoplegia, homonymous visual field defects, dysarthria, vertebral bruits, and ataxia proximal May cause dizzyness extracranial occlusion of the vertebral aa Basilar artery occlusion subclavian steal May cause dizzyness syndrome. PICA blockage: May cause acute severe vertigo due to cerebellar infarction. Lateral Medullary Syndrome Dysfunction Effects vestibular nuclei inferior cerebellar peduncle vestibular system: vomiting, vertigo, nystagmus, Ipsilateral cerebellar signs including ataxia, dysmetria (past pointing), dysdiadokokinesia contralateral deficits in pain and temperature sensation from body (limbs and torso)

lateral spinothalamic tract

spinal trigeminal nucleus & ipsilateral loss of pain, and temperature sensation tract from face nucleus ambiguus - (which affects vagus nerve and glossopharyngeal nerve - ipsilateral laryngeal, pharyngeal, and palatal localizing lesion (all other hemiparalysis: dysphagia, hoarseness, diminished deficits are present in gag reflex (efferent limb - CN.X) lateral pontine syndrome as well) descending sympathetic fibers ipsilateral Horner's syndrome (ptosis, miosis, & anhydrosis)

Carotid artery stenosis Basilar type migraine TUMOURS cerebellopontine angle

Posterior fossa lesions Acoustic neuroma

Usually a schwanoma on CNVIII within int. auditory canal. May also be meningiomas, epidermoids and metastases. Rarely present solely with episodic vertigo, as tumour enlarges it may press on acoustic part of CNVIII, CNVII, CNV brainstem and cerebellum s- progressive hearing loss and tinnitus. Vertigo in approx. 20%, but imbalance or disequilibration is more common. Signs: must test CNV, CNVII inc. corneal reflex Agg by changes in head position s- may include oscillopsia, an illusion of environmental movement characterized by bouncing or jiggling of objects ( this may also be due to drugs) Check for upbeat/ down beat nystagmus Vertigo lasts for hours at a time. Pain over mastoid/ ear, facial weakness, H/A, hearing loss, tinnitus a typical headache (often throbbing, unilateral, sometimes preceded by an aura), nausea, vomiting, photophobia, and phonophobia. Twenty-one to 35 percent of patients with migraine suffer vertigo. nonsyphilitic keratitis associated with vertigo, tinnitus, ataxia, nystagmus, rapidly progressive deafness, and systemic involvement rare causes of dizziness or vertigo

Migraine

Cogans syndrome Seizure disorders esp complex partial epilepsy Multiple sclerosis

disseminated CNS lesions such as optic neuritis, transverse myelitis, internuclear ophthalmoplegia or other brainstem signs Agg by changes in head position but also spontaneous episodes

Cervical spondylosis Medications/ intoxication CO poisoning Cerebellar lesion Closed head injury

Vertigo, nystagmus, gait, no hearing affected, neurological signs (ipsilateral)

SYSTEMIC DISEASE Vasculitis e.g. collagen vascular disease (Marfans, SLE), GCA, drug induced Granulomatous disease (TB) Meningeal carcinomatosis Hyperventilation Drugs Hypotension, presyncope

May result in cranial neuropathy

May result in cranial neuropathy May result in cranial neuropathy anxiety including anticonvulsants, hypnotics, antihypertensives, alcohol, analgesics, tranquillizers Postural hypotension is a common side effect of antihypertensive agents, diuretics, and dopaminergic agents. When the symptom is intermittent, a history of lightheadedness following change from recumbent or sitting posture to an erect position, but not the reverse, is more helpful than blood pressure measurements. In adolescents, a hyposensitive carotid sinus reflex during the growth spurt is not rare, and transient symptoms of postural dizziness might be explained by this mechanism Check CVS (including syphilis, viral and other bacterial meningitides, and systemic infection) including diabetes ( due to neuropathy) and hypothyroidism polycythemia, anemia and dysproteinemia vision (cataracts), hearing (presbycusis), and proprioception (peripheral neuropathy) may all be impaired. There is an entity known as presbylibrium or imbalance resulting from aging which may be due to a selective progressive deterioration of the peripheral vestibular apparatus

Infectious diseases Endocrine hematological disorders, Old age

or a combination of sensory deficits.

Tests Refer for an electronystagmogram (ENG) to measure (a) documentation of spontaneous and induced nystagmus, (b) quantitation of fast eye movements, (c) smooth pursuit tracking, (d) optokinetic responses, and (e) gaze testing. Posturography/ rotation tests Also blood count, electrolytes, glucose and thyroid function testing, lipid screens for the presence of hypercholesterolemia or increased triglycerides. Cardiac evaluation inc. ECG or a Holter 24-hour monitor or an event monitor Audiological evaluation Multiple or recurrent cranial neuropathy would lead to a variety of screening tests for collagen vascular disease or skull-based pathology or meningitic processes. CT/ MRI scans

Medication Antihistamines Meclizine 25-50 mg 3 times/day- most common S/E drowsiness Cyclizin50 mg 1 - 2 times/day Dymenhydrinate/td>50 mg 1 - 2 times/day Promethazine25 - 50 mg/day Scopolamine 1 three times/day Ephedrine 25 mg/day Trimethobenzamide 250 mg 1 - 2 times/day orally/200 mg suppository Promethazine25 - 50 mg/day/5 - 10 mg 3 - 4 times/day orally Diazepam 5 - 10 mg 1 - 3 times/day Serax10 - 60 mg/day Haloperidol***0.5 - 1 mg 1 - 2 times/day Verapamil 80 mg 1 -3 times/day Buclazine, Cyclandelate, Diuretics, Diet

Anticholinergics Sympathomimetics Antiemetics Tranquilizers

Calcium Channel Blockers Others