HEADACHE

Headaches
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 - usually benign in course and

long-term outcome

 Secondary headaches - frequently due to structural lesions

and are guarded in prognosis
 Pain-sensitive structures of the head and neck

Cervical spine
Teeth
Paranasal sinuses
Extracranial structures
Eyes
Scalp and extracranial muscles
Extracranial arteries
Facial bones

Periostium
Venous sinuses Intracranial structures
Meninges
Intracranial arteries
 Pain-sensitive structures of the head and neck

Cervical spine spondylosis, disc lesions,whiplash injury

Teeth apical tooth abscess
Paranasal sinuses sinusitis
Eyes acute glaucoma, uveitis, retrobulbar neuritis
Scalp and extracranial muscles trauma
Extracranial arteries giant cell arteritis
Facial bones TMJ dysfunction

Periostium Osteomyelitis, Paget’s disease

Venous sinuses Venous sinus thrombosis
Meninges SAH, Meningitis
Intracranial arteries Malignant hypertension, Hypercapnia
Consider the following in the history:
o mode of onset - acute, subacute, chronic, recurrent and episodic

o subsequent course - episodic, progressive, chronic and persistent

o site - unilateral or bilateral

- frontal, temporal, occipital
- radiation to the neck, arm, or shoulder

o character - constant, throbbing, stabbing, dull, pressure-like

o frequency and duration

o accompanying features - neck stiffness, autonomic symptoms

o exacerbating factors - movement, light, noise, smell

- coughing, sneezing, bending
Consider the following in the history:

o precipitating factors - alcohol, stress, postural changes, head injury

oparticular time of onset - mornings, awaken at night

o past history of headaches - “chronic headaches are frequently benign”

o family history - migraine, hypertension, stroke

o general health - systemic illness, existing medical conditions

o drug history - 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
Migraine Unilateral throbbing headache exacerbated by movement
Accompanied by nausea, vomiting, photo-, phonobobia
+/- aura symptoms

Cluster headache 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

Trigeminal Neuralgia 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

Benign Precipitated by exertion, coughing, straining and orgasms

exertional/cough May be benign, but more of a diagnosis by exclusion

headaches
Paroxysmal This occurs in cases of pheochromocytoma
hypertension
Intermittent Intermittent severe headaches accompanied by “drop attacks”,
weakness of legs and unsteady gait
hydrocephalus
 Chronic Daily Headaches

Causes Clinical Features

Transformed Migraine +/- Daily, mild, bilateral, usually featureless headaches with superimposed
episodes of characteristic migraine headaches
analgesic overuse

Tension-type headache Bilateral featureless headache, usually episodic

+/- analgesic overuse Band-like pain on temporofrontal area

Postherpetic neuralgia 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 Post-traumatic syndrome includes:

• post-concussional headache
headaches
• episodic migrainous headaches
• daily occurrence
• tenderness or pain at the site of the truma
• occipital or neck pain from upper cervical injuries

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 Clinical features

Intracranial tumor Excerbated by coughing, straining, sneezing, may occur with obstruction
of the CSF pathways
Seizures, focal neurological deficits (depeding on the site of the tumor)

Chronic meningitis Tuberculous focus present; cryptococcal meningitis;

syphilitic

Giant-cell arteritis 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

Intracranial abscess Direct extension from local disease

Fever, systemic manifestations, focal neurological deficits

Subdural hematoma +/- head injury (elderly and alcoholics); fluctuating level of
consciousness; confusion; focal neurological signs

Benign intracranial Young, overweight females

hypertension Papilledema; raised CSF pressure
CT/MRI may be normal, although lateral ventricles are usually small
 Acute-onset headache

Cause Clinical features

Subarachnoid Explosive-onset “thunderclap” headache
hemorrhage Neck stiffness, photophobia, meningeal signs
+/- focal neurological deficits if with intracerebral extension

Cerebral hemorrhage History of hypertension or pt under anticoagulant

Focal neurological deficits (depending on the site of hematoma)

Meningitis / encephalitis +/- history of systemic infection

Fever, neck stiffness, +/- meningeal signs

Acute hydrocephalus Nausea, vomiting, diplopia; cranial nerve deficits

+/- papilledema’ ataxia of gait

Hypertensive crisis Very high blood pressure; papilledema may be present

Acute glaucoma Pain typically frontal, orbital or ocular; accompanied by persistent visual
impairment; fixed oval pupil and conjunctival injection
(this is ophthalmologic emergency)

Migraine of cluster Migraine can also present as sudden severe headache (thunderclap), the
diagnosis of migraine will then be by exclusion unless recurrent
headache – first episode 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 Emotional Stress

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

¤ 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
Demyelinating Diseases
• Vestibular Nerve lesions Neoplastic infiltration
Vestibular neuronitis
• Cerebellar diseases
• Cerebellopontine angle lesions
Acoustic neuroma
Granulomatous diseases
Vascular lesions
 Lesion Localization in a Patient Presenting with Vertigo

Labyrynthine failure Vestibular Nerve Cerebellopontine

lesion angle lesion
Vertigo Common may be prolonged Rare
Short attacks

Nystagmus Horizontal and/or rotary Horizontal and/or rotary Horizontal

(opposite to lesion) (opposite to lesion)
(fast phase) (towards lesion)

Gait Veers toward the lesion Veers toward the lesion Ataxia on side of the
lesion; may have
hemiparesis

Hearing Conductive or Sensorineural loss Sensorineural high pitch

sensorineural loss loss early

Other signs none +/- 7th nerve or 5th nerve 5th, 7th, 9th, 10th nerve lesion
lesions Ipsilateral cerebellar signs
Contralateral pyramidal
signs
 Lesion Localization in a Patient Presenting with Vertigo

Brainstem lesions Cerebellar lesions

Vertigo May be prolonged Brainstem connections involved

Nystagmus Vertical nystagmus Horizontal (coarse)

(fast phase) (towards the lesion)

Gait Hemiparesis Ataxia on side of the lesion

Hearing Usually unaffected Unaffected

Other signs Ipsilateral cranial nerve Unilateral cerebellar signs from an

palsies ipsilateral cerebellar hemispheric lesion
Contralateral pyramidal
involvement
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)

XII. 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