The approach to a patient with headache should be based on the temporal pattern of symptoms, especially the mode of onset and subsequent course  recurrent and episodic  chronic and daily  subacute onset  acute onset

Based on the temporal occurrence of the headache, one must bear in mind:  Primary headaches  Secondary headaches - usually benign in course and long-term outcome - frequently due to structural lesions and are guarded in prognosis

Pain-sensitive structures of the head and neck
Cervical spine Teeth Paranasal sinuses Eyes Scalp and extracranial muscles Extracranial arteries Facial bones

Extracranial structures

Periostium Venous sinuses Meninges Intracranial arteries

Intracranial structures

Pain-sensitive structures of the head and neck
Cervical spine Teeth Paranasal sinuses Eyes Scalp and extracranial muscles Extracranial arteries Facial bones spondylosis, disc lesions,whiplash injury apical tooth abscess sinusitis acute glaucoma, uveitis, retrobulbar neuritis trauma giant cell arteritis TMJ dysfunction

Periostium Venous sinuses Meninges Intracranial arteries

Osteomyelitis, Paget’s disease Venous sinus thrombosis SAH, Meningitis Malignant hypertension, Hypercapnia

Consider the following in the history:
o mode of onset o subsequent course o site - acute, subacute, chronic, recurrent and episodic - episodic, progressive, chronic and persistent - unilateral or bilateral - frontal, temporal, occipital - radiation to the neck, arm, or shoulder - constant, throbbing, stabbing, dull, pressure-like

o character o frequency and duration o accompanying features o exacerbating factors

- neck stiffness, autonomic symptoms - movement, light, noise, smell - coughing, sneezing, bending

Consider the following in the history:
o precipitating factors oparticular time of onset - alcohol, stress, postural changes, head injury - mornings, awaken at night

o past history of headaches - “chronic headaches are frequently benign” o family history o general health o drug history - migraine, hypertension, stroke - systemic illness, existing medical conditions - analgesics, recreational drugs, drugs for the existing medical problems

Don’t miss the following in the physical examination:
 look for focal neurological signs (the presence of which almost always indicate secondary type of headache!)  signs of local disease of the extracranial structures signs of neck movement restrictions  thickening of the temporal arteries (temporal arteritis)  signs of systemic disease/s  abnormal blood pressure (systemic hypotension can cause traction on the pain-sensitive structures in the cranial vault)

Recurrent Episodic Headaches Causes

Clinical Features
Unilateral throbbing headache exacerbated by movement Accompanied by nausea, vomiting, photo-, phonobobia +/- aura symptoms Severe unilateral retro-orbital, +/- temporal pain Ipsilateral conjunctival injection, lacrination, partial Horner’s syndrome, rhinorhea, nasal blockage Attacks last 15min to several hours, occur several times in a day for about 2-3 months interval Jabs of severe unilateral pain in the 2nd and 3rd distribution of the CN V Triggered by actions such as chewing, brushing of teeth, talking, cold wind Precipitated by exertion, coughing, straining and orgasms May be benign, but more of a diagnosis by exclusion

Cluster headache

Trigeminal Neuralgia

Benign exertional/cough headaches Paroxysmal hypertension Intermittent hydrocephalus

This occurs in cases of pheochromocytoma

Intermittent severe headaches accompanied by “drop attacks”, weakness of legs and unsteady gait

Chronic Daily Headaches Causes
Transformed Migraine +/analgesic overuse Tension-type headache +/- analgesic overuse Postherpetic neuralgia

Clinical Features
Daily, mild, bilateral, usually featureless headaches with superimposed episodes of characteristic migraine headaches Bilateral featureless headache, usually episodic Band-like pain on temporofrontal area After an attack of herpes zoster there may be continuous burning pain with superimposed occasional stabs in the distribution of the affected nerve distribution (dermatomes) Post-traumatic syndrome includes: • post-concussional headache • episodic migrainous headaches • daily occurrence • tenderness or pain at the site of the truma • occipital or neck pain from upper cervical injuries

Post-traumatic headaches

Atypical facial pains

Constant aching pain in the lower part of the face commonly occurs in women; may follow a minor facial injury or dental procedure

Subacute-onset headache Causes
Intracranial tumor Chronic meningitis Giant-cell arteritis

Clinical features
Excerbated by coughing, straining, sneezing, may occur with obstruction of the CSF pathways Seizures, focal neurological deficits (depeding on the site of the tumor) Tuberculous focus present; cryptococcal meningitis; syphilitic Patients usually over 50 years, female preponderance Visual disturbances – ischemic papillopathy Associated with polymyalgia rheumatica Elevated ESR Tender, thickened temporal artery; giant-cell arteritis on biopsy Direct extension from local disease Fever, systemic manifestations, focal neurological deficits +/- head injury (elderly and alcoholics); fluctuating level of consciousness; confusion; focal neurological signs Young, overweight females Papilledema; raised CSF pressure CT/MRI may be normal, although lateral ventricles are usually small

Intracranial abscess Subdural hematoma Benign intracranial hypertension

Acute-onset headache Cause
Subarachnoid hemorrhage Cerebral hemorrhage Meningitis / encephalitis Acute hydrocephalus Hypertensive crisis Acute glaucoma Migraine of cluster headache – first episode

Clinical features
Explosive-onset “thunderclap” headache Neck stiffness, photophobia, meningeal signs +/- focal neurological deficits if with intracerebral extension History of hypertension or pt under anticoagulant Focal neurological deficits (depending on the site of hematoma) +/- history of systemic infection Fever, neck stiffness, +/- meningeal signs Nausea, vomiting, diplopia; cranial nerve deficits +/- papilledema’ ataxia of gait Very high blood pressure; papilledema may be present Pain typically frontal, orbital or ocular; accompanied by persistent visual impairment; fixed oval pupil and conjunctival injection (this is ophthalmologic emergency) Migraine can also present as sudden severe headache (thunderclap), the diagnosis of migraine will then be by exclusion unless recurrent episodes have occurred in the past

Headache Danger Signals on History  Sudden-onset of new severe headache  progressively worsening headaches  onset with exertion, coughing, straining, and/or sexual activity  onset of headache after the age of 50 years  associated symptoms such as:      drowsiness chronic malaise, myalgia, arthralgia fever progressive visual disturbances weakness, clumsiness, loss of balance

Headache Danger Signals on Examination  abnormal vital signs especially fever or hypertension  altered level of consciousness  meningeal irritation  papilledema or fundal hemorrhages  unequal pupils  weakness or sensory loss in the face or limbs  reflex asymmetry or abnormal plantar response  clumsiness or loss of balance  tender, poorly-pulsatile cranial arteries

International Headache Society Diagnostic Criteria
Headache Classification Committee of the International Headache Society; Classification and Diagnosis Criteria of Headache Disorders, Cranial Neuralgias, and Facial Pain; Cephalgia, 1988: 8 supplement 7: 1-96

Migraine with aura
o also known as Classic Migraine o two or more headache attacks preceded by neurological symptoms (aura) which have ff. characteristics: i. aura symptoms usually involving visual disturbances such as blurring, flashing lights, missing chunks of visual fields, must be fully reversible ii. Aura develops gradually over at least 5 minutes, and lasts for about less than 60 minutes o headache must follow aura within 60 minutes of remission

International Headache Society Diagnostic Criteria
Headache Classification Committee of the International Headache Society; Classification and Diagnosis Criteria of Headache Disorders, Cranial Neuralgias, and Facial Pain; Cephalgia, 1988: 8 supplement 7: 1-96

Migraine without aura
o also known as Common Migraine o five or more headache attacks lasting 4-72 hours: o the headaches must have two of the ff. characteristics i. localized on one side of the head ii. Pulsating iii. Severe enough to inhibit daily activity iv. Aggravated by physical activity o headache must be accompanied by either nausea and/or vomiting or photophobia and phonophobia

Migraine Triggers
Hormonal or systemic factors  menstruation  ovulation Contraceptive pills  high blood pressure Diet Physical stress Red wine  phenylethylamine (Chocolates)  tyramine (cheese, nuts)  monosodium glutamate  nitrites  caffeine/caffeine withdrawal  octopamine (citrus fruits)  skipping meals  over exertion  physical or mental fatigue  sleep – too much and too little  travel  sexual activity Emotional Stress  depression  shock  excitement  anxiety  heightened emotion

International Headache Society Diagnostic Criteria
Headache Classification Committee of the International Headache Society; Classification and Diagnosis Criteria of Headache Disorders, Cranial Neuralgias, and Facial Pain; Cephalgia, 1988: 8 supplement 7: 1-96

Tension-type headache
o ten or more headaches attacks lasting between 30 min. to 7 days o the headaches must have two of the ff. characteristics i. pain is pressing / tightening (not throbbing) ii. Mild to moderate in intensity (not severe enough to inhibit daily activity) iii. Pain present on both sides of the head iv. No aggravation of pain by physical activity o no nausea or vomiting o photophobia and phonophobia may occur, but not together

International Headache Society Diagnostic Criteria
Headache Classification Committee of the International Headache Society; Classification and Diagnosis Criteria of Headache Disorders, Cranial Neuralgias, and Facial Pain; Cephalgia, 1988: 8 supplement 7: 1-96

Cluster Headache
o at least 5 attacks of severe pain lasting 15-180 minutes o attacks occur up to 8 times a day in clusters lasting for a week or months o pain localized above the eyes or in the temples, on one side of the head only o headache must be associated on pain side: conjunctivitis, lacrimation, nasal congestion, rhinorhea, facial sweating, eyelid edema, miosis and ptosis

MIGRAINOUS NEURALGIA(Cluster headache). Horner’s syndrome during an attack.

OPHTHALMOPLEGIC MIGRAINE. There is a right ptosis.

Dizziness and Vertigo
Dizziness - a term that patient may use to describe vertigo, faintness, disorientation, drowsiness, light-headedness, visual disturbances or even legs unsteadiness Vertigo - illusion or hallucination of movement - the perceived movement may be rotational, swaying, rocking, or heaving in quality

¤ vertigo is either peripheral or central ¤ vertigo from supranuclear lesion is uncommon, therefore the main consideration would be between a. a peripheral lesion (labyrinthine, vestibular nerve or ganglion) b. brainstem lesion c. cerebellar lesion ¤ vertigo is usually not the sole manifestation of a brainstem disease – always look for ipsilateral cranial nerve deficits and contralateral pyramidal signs ¤ in vertigo due to cerebellar lesions, there may be signs of ipsilateral incoordination which are absent in peripheral vestibular lesions ¤ vertigo may be the sole manifestation of vestibular dysfunction, this can be confirmed by neuro-otological testings

Differential Diagnosis of Vertigo

• Labyrinthine failure

Meniere’s disease Benign Positional Vertigo Labyrinthitis • Brainstem lesions Motion sickness Brainstem stroke syndrome
• Vestibular Nerve lesions

Vestibular neuronitis
• Cerebellopontine angle lesions

Demyelinating Diseases Neoplastic infiltration • Cerebellar diseases

Acoustic neuroma Granulomatous diseases Vascular lesions

Lesion Localization in a Patient Presenting with Vertigo
Labyrynthine failure Vestibular Nerve lesion
may be prolonged Horizontal and/or rotary (opposite to lesion) Veers toward the lesion

Cerebellopontine angle lesion
Rare Horizontal (towards lesion)

Vertigo Nystagmus (fast phase) Gait Hearing Other signs

Common Short attacks Horizontal and/or rotary (opposite to lesion) Veers toward the lesion

Ataxia on side of the lesion; may have hemiparesis Sensorineural high pitch loss early 5th, 7th, 9th, 10th nerve lesion Ipsilateral cerebellar signs Contralateral pyramidal signs

Conductive or sensorineural loss none

Sensorineural loss +/- 7th nerve or 5th nerve lesions

Lesion Localization in a Patient Presenting with Vertigo
Brainstem lesions Cerebellar lesions
Brainstem connections involved Horizontal (coarse) (towards the lesion) Hemiparesis Usually unaffected Ipsilateral cranial nerve palsies Contralateral pyramidal involvement Ataxia on side of the lesion Unaffected Unilateral cerebellar signs from an ipsilateral cerebellar hemispheric lesion

Vertigo Nystagmus (fast phase) Gait Hearing Other signs

May be prolonged Vertical nystagmus

Investigations in cases of vertigo

The Hallpike maneuver • performed with patient sitting on a bed, and asked to fall backwards so that his head is below the plane of his body • the positioned head is turned 30 degrees to the affected side and the patient is asked to look to the turned side • after a latent period of few seconds, vertigo may be experienced • there’s accompanying torsional nystagmus with upper pole beating towards the floor • the direction of the nystagmus are reversed on sitting up again in peripheral (labyrinthine) lesions, symptoms and signs last for about 30 sec. and fatigue with repetition such that they cannot then be reproduced

Investigations in cases of vertigo

The Caloric testing • with the patient in lying position, head is raised 30 degrees, so that the horizontal canals are vertical • each external meatus is irrigated for 30 sec with cold and warm water normal response: “COWS” canal paresis (peripheral lesion): no response to irrigation of the external meatus eg. Labyrinthine lesions Nerve lesions Vestibular ganglion lesion directional preponderance eg. Brainstem vestibular nuclei lesion

Limb Weakness

Weakness in the limbs can result from pathology anywhere along the UMN pathway (cortex,
subcortical fibers, brainstem, spinal cord),

from lesions in the LMN (anterior horn cells,
nerve roots, plexus, peripheral nerves) or

from disorders arising from the NMJ or the muscles

Patterns of motor weakness due to UMN lesions
III. Spastic hemiparesis and ipsilateral facial weakness hemispheric cortex: aphasia (dominant hemisphere) involvement of the face and arm alone, or leg alone, depending on the site of the lesion internal capsule: dense hemiplegia upper brainstem: upper cranial nerve palsies certain characteristic sensory changes

Patterns of motor weakness due to UMN lesions

II. Spastic hemiparesis and contralateral facial weakness Lower brainstem involvement
Lower cranial nerve palsies and certain characteristic sensory changes

III. Spastic hemiparesis sparing the face Unilateral upper cervical cord lesions
Brown-Sequard syndrome

Patterns of motor weakness due to UMN lesions
IV. Spastic quadriparesis Lower brainstem lesions
Lower cranial nerve palsies depending on the site of the lesion

High cervical cord lesions
No cranial nerve deficits Loss of sensory modalities below the site of the lesion

V. Spastic Paraparesis Thoracic cord lesions
Loss of all sensory modalities below the level of the lesion

VI. Spastic monoparesis Unilateral thoracic cord lesion
Brown-Sequard syndrome at the thoracic level

Pattern of LMN weakness
III. Anterior Horn Cell diseases - may be diffused or confined to restricted group of muscles - causes:
genetic (Spinal muscular atrophy) Idiopathic (ALS) Infectious (Poliomyelitis) Toxic (chemical exposure, eg. Triorthocresylphosphate)


Radiculopathy (root lesions) and Plexopathy (plexus lesions) - a root lesion will cause muscle weakness in the corresponding myotome - if the dorsal roots are also involved, there will be accompanying sensory loss in defined dermatomal distribution - a plexus lesion will cause weakness in muscles innervated by a number of nerve roots which comprise the plexus - accompanying sensory loss over several dermatomes may be present

Pattern of LMN weakness
III. Radiculopathy and Plexopathy Examples of Plexopathies Brachial Plexus 1. Erb’s palsy (C5-6) - upper plexus injury (loss of shoulder abduction and elbow flexion 2. Klumpke’s palsy (C8-T1) - lower plexus injury (loss of function of the intrinsic muscles of the hand and long flexors and extensors of the fingers) 3. Thoracic outlet syndrome - the brachial plexus and the subclavian artery are compressed by fibrous band or a cervical rib 4. Neuralgic amyotrophy - acute brachial plexus neuropathy which may follow infections, vaccination, or surgery; accompanied by severe pain

Pattern of LMN weakness
IV. Radiculopathy and Plexopathy Lumbosacral Plexus Lesions in the lumbosacral plexus includes:
trauma following abdominal surgery or pelvic surgery neoplastic infiltration granulomatous lesions compression due to aortic aneurysm

Pattern of LMN weakness
III. Disorders of the peripheral nerves 1. Mononeuropathy - disease of a single peripheral nerve eg. Carpal Tunnel syndrome 2. Multifocal neuropathy (Mononeuropathy multiplex) - many single peripheral nerves are involved eg. Diabetic neuropathy, Sarcoidosis, Leprosy 3. Polyneuropathy (Peripheral neuropathy) - more widespread involvement of the peripheral nerves - typically in a symmetric distal distribution eg. GBS, Vit B12 deficiency

Pattern of LMN weakness
IV. Disorders of the neuromuscular junction (NMJ)

Myasthenia gravis Lambert-Eaton Myasthenic Syndrome Botulism Drug-induced NMJ malfunction - the weakness predominantly affects the proximal muscles - may be become widespread in advanced stages - in myasthenia, ocular muscles are characteristically affected - the outstanding feature: easily fatiguable muscles - wasting is relatively uncommon; reflexes are frequently normal

Pattern of LMN weakness
V. Disorders of muscles - in myopathies, limb weakness is bilateral and proximal in the upper and/or lower limbs - muscle wasting may be severe and is restricted to the weak muscle groups - tone is reduced and is proportional to the muscle wasting Examples of Myopathies: Progressive Muscular Dystrophies (Duchenne) Inflammatory Myopathies (Polymyositis)

Disorders of Gait

When assessing gait, the ff. categories should be kept in mind: Cerebellar ataxia Spastic Gait Parkinsonian gait Steppage agit Myopathic gait Apraxic gait Hysterical gait The character of the gait will provide clues to the clinical signs that might Be expected on further neurological evaluation

Gait of cerebellar ataxia
• patient stands and walks on a wide-based gait (the feet spaced widely apart) • the gait is unsteady, with irregularity of stride • the trunk sways and the patient may veer towards one side • in mild cases, the only manifestation of gait disturbance may be difficulty walking heel-toe in a straight line • always look for cerebellar signs in the limbs; ataxia of gait may be the only sign of cerebellar dysfunction (midline cerebellar lesions

Causes of cerebellar ataxia: Multiple Sclerosis Alcoholic Cerebellar Degeneration Anticonvulsant therapy Posterior Fossa Tumors Cerebellar Paraneoplastic Syndromes Hereditary Cerebellar Ataxias

emiparetic Gait

here is a characteristic posture on one side (flexion of the upper limb and extension on the lower limb

he extended lower limb moves stiffly and is swung round in a semicircle to avoid scraping the foot across the floor (the outer sole of the shoe is become worn)

Causes: Cerebral hemispheric stroke syndromes Infiltrating neoplasms (Glioblastoma multiform Traumatic Head Injury

stic Gait

n in patients who have spastic paraparesis or bilateral hemiplegia legs move slowly and stiffly, the thighs are strongly adducted such that the legs may cross as the patient walks (scissor gait)

Causes include:

Spinal Cord diseases / compression Spinal trauma or surgery Birth injuries or congenital deformities (eg Cerebral Palsy, Spina bifida) Multiple Sclerosis (MS) Motor neuron Diseases (eg ALS, Primary lateral Sclero Scler Parasaggital meningiomas Subacute Combined Degeneration of the Cord

Parkinsonian Gait
• stooped posture and loss of arm swing • steps are short and the shuffling (festinating gait) • there may be difficulty starting, stopping, and turning • having started walking, patient leans forward and the pace quickens, as though the patient has to catch up on himself

Gait of Sensory Ataxia
• due to impaired proprioception by lesions involving the peripheral nerves, posterior root, dorsal columns of the spinal cord, or the ascending fibers to the parietal lobes • the gait is “stamping” (shoe soles are equally worn out)

Causes include: Posterior Spinal Cord lesions Vit. B12 deficiency Tabes dorsalis Cervical Spondylosis MS Sensory Peripheral Neuropathies include: Hereditary - Charcot-Marie-Tooth disease Metabolic - Diabetic Neuropathy Inflammatory - GBS Malignancy - paraneoplstic Syndrome Toxic - alcohol, drugs

Steppage Gait
• arises from weakness of the pretibial and peroneal muscles of the LMN-type • patient has “footdrop” and is unable to dorsiflex and evert the foot • the leg is lifted high on walking so that the toes clear the ground • on striking the floor, there is “slapping” noise (shoe soles are worn in the anterior and lateral aspects)

Causes: Charcot-Marie-Tooth disease (bilateral footdrop) Fibular fracture (lateral popliteal nerve palsy) Anterior horn cell disease (Poliomyeltis)

Myopathic Gait
• waddling gait; due to weakness of the proximal muscles of the lower limb girdle • the weight is alternately placed on each leg, with the opposite hip and one side of the trunk tilting up towards the weight-bearing side, the weak gluteal muscles cannot stabilize the weight-bearing hip

Causes: Muscular Dystrophies (eg. Duchenne, Becker’s) Endocrine Myopathies (eg Cushing’s Disease) Metabolic Myopathies (eg. Periodic paralysis) Inflammatory Myopathies

Apraxic gait
• Walks with feet placed apart, and with small, hesitant steps • “walking on ice” • there is difficulty initiation of walking, and with advances cases, as if the the patient is stuck to the floor • due to frontal lobe disease; look for primitive frontal reflexes

Causes: Bilateral subcortical stroke Normal-pressure hydrocephalus Alzheimer diseases Frontal Subdural hematoma Frontal lobe tumors

Antalgic gait
• arises from pain (painful hip or knee) due to arthritis •Patient tend to weight-bear mainly on the affected side • tendency to hobble

Hysterical gait
• does not conform to any of the mentioned abnormal gait • may take a number of forms and is variable in character • no abnormal formal neurological deficits

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