Headache ppt

HEADACHE

Headaches

The approach to a patient with headache should be basedon the temporal pattern of symptoms, especially the modeof 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:Based on the temporal occurrence of the headache, one must bear in mind:

Primary headaches Primary headaches - usually benign in course and - usually benign in course and long-term outcomelong-term outcome

Secondary headaches - frequently due to structural lesionsSecondary headaches - frequently due to structural lesionsand are guarded in prognosisand are guarded in prognosis

Pain-sensitive structures of the head and neck

Cervical spineTeeth Paranasal sinusesEyesScalp and extracranial musclesExtracranial arteriesFacial bones

PeriostiumVenous sinusesMeningesIntracranial arteries

Extracranial structures

Intracranial structures

Pain-sensitive structures of the head and neck

Cervical spine spondylosis, disc lesions,whiplash injuryTeeth apical tooth abscessParanasal sinuses sinusitisEyes acute glaucoma, uveitis, retrobulbar neuritisScalp and extracranial muscles traumaExtracranial arteries giant cell arteritisFacial bones TMJ dysfunction

Periostium Osteomyelitis, Paget’s diseaseVenous sinuses Venous sinus thrombosisMeninges SAH, MeningitisIntracranial 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 theexisting medical problems

Don’t miss the following in the physical examination:

look for focal neurological signs (the presence of which almostalways 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-, phonofobia

+/- 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 exertional/cough headaches

Precipitated by exertion, coughing, straining and orgasms

May be benign, but more of a diagnosis by exclusion

Paroxysmal hypertension

This occurs in cases of pheochromocytoma

Intermittent hydrocephalus

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

Chronic Daily Headaches

Causes Clinical Features

Transformed Migraine +/- analgesic overuse

Daily, mild, bilateral, usually featureless headaches with superimposed episodes of characteristic migraine headaches

Tension-type headache +/- analgesic overuse

Bilateral featureless headache, usually episodic

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 headaches

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

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 hypertension

Young, overweight females

Papilledema; raised CSF pressure

CT/MRI may be normal, although lateral ventricles are usually small

Acute-onset headache

Cause Clinical features

Subarachnoid hemorrhage

Explosive-onset “thunderclap” headache

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 headache – first episode

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 FacialPain; Cephalgia, 1988: 8 supplement 7: 1-96

Migraine with aura

o also known as Classic Migraineo 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 visualfields, must be fully reversible

ii. Aura develops gradually over at least 5 minutes, and lasts forabout less than 60 minutes

o headache must follow aura within 60 minutes of remission



Migraine without aura

o also known as Common Migraineo 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 headii. Pulsatingiii. Severe enough to inhibit daily activityiv. 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 ovulationContraceptive pills high blood pressure

Diet

Red wine phenylethylamine (Chocolates) tyramine (cheese, nuts) monosodium glutamate nitrites caffeine/caffeine withdrawal octopamine (citrus fruits) skipping meals

Emotional Stress

depression shock excitement anxiety heightened emotion

Physical stress

over exertion physical or mental fatigue sleep – too much and too little travel sexual activity



Tension-type headache

o ten or more headaches attacks lasting between 30 min. to 7 dayso 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 headiv. No aggravation of pain by physical activity

o no nausea or vomitingo photophobia and phonophobia may occur, but not together



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, miosisand 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 lesionc. cerebellar lesion

¤ vertigo is usually not the sole manifestation of a brainstem disease – always lookfor ipsilateral cranial nerve deficits and contralateral pyramidalsigns

¤ in vertigo due to cerebellar lesions, there may be signs of ipsilateralincoordination which are absent in peripheral vestibular lesions

¤ vertigo may be the sole manifestation of vestibular dysfunction, this can beconfirmed by neuro-otological testings

• Labyrinthine failureMeniere’s diseaseBenign Positional VertigoLabyrinthitisMotion sickness

• Vestibular Nerve lesionsVestibular neuronitis

• Cerebellopontine angle lesionsAcoustic neuromaGranulomatous diseasesVascular lesions

Differential Diagnosis of Vertigo

• Brainstem lesionsBrainstem stroke syndromeDemyelinating DiseasesNeoplastic infiltration

• Cerebellar diseases

Lesion Localization in a Patient Presenting with Vertigo

Labyrynthine failure Vestibular Nerve lesion

Cerebellopontine angle lesion

Vertigo Common

Short attacks

may be prolonged Rare

Nystagmus

(fast phase)

Horizontal and/or rotary

(opposite to lesion)

Horizontal and/or rotary

(opposite to lesion)

Horizontal

(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 loss Sensorineural high pitch loss early

Other signs none +/- 7th nerve or 5th nerve lesions

5th, 7th, 9th, 10th nerve lesion

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

(fast phase)

Vertical nystagmus Horizontal (coarse)

(towards the lesion)

Gait Hemiparesis Ataxia on side of the lesion

Hearing Usually unaffected Unaffected

Other signs Ipsilateral cranial nerve palsies

Contralateral pyramidal involvement

Unilateral cerebellar signs from an ipsilateral cerebellar hemispheric lesion

Investigations in cases of vertigo

The Hallpike maneuverThe Hallpike maneuver

• performed with patient sitting on a bed, and asked to fall backwards so thathis head is below the plane of his body

• the positioned head is turned 30 degrees to the affected side and thepatient 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 forabout 30 sec. and fatigue with repetition such thatthey cannot then be reproduced

Investigations in cases of vertigo

The Caloric testingThe Caloric testing

• with the patient in lying position, head is raised 30 degrees, so that thehorizontal 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 lesionsNerve lesionsVestibular ganglion lesion

directional preponderanceeg. Brainstem vestibular nuclei lesion

Limb Weakness

Weakness in the limbs Weakness in the limbs can result from can result from pathology anywhere pathology anywhere along the UMN along the UMN pathway pathway (cortex, (cortex, subcortical fibers, subcortical fibers, brainstem, spinal cord),brainstem, spinal cord), from lesions in the from lesions in the LMN LMN (anterior horn cells, (anterior horn cells, nerve roots, plexus, nerve roots, plexus, peripheral nerves)peripheral nerves) or or from disorders arising from disorders arising from the NMJ or the from the NMJ or the musclesmuscles

Patterns of motor weakness due to UMN lesionsPatterns of motor weakness due to UMN lesions

I. Spastic hemiparesis and ipsilateral facial weakness

hemispheric cortex:hemispheric cortex:

aphasia (dominant hemisphere)involvement of the face and arm alone, orleg alone, depending on the site of the lesion

internal capsule:internal capsule:

dense hemiplegia

upper brainstem:upper brainstem:

upper cranial nerve palsiescertain characteristic sensory changes


II. Spastic hemiparesis and contralateral facial weakness

Lower brainstem involvementLower brainstem involvement

Lower cranial nerve palsies andcertain characteristic sensory changes

III. Spastic hemiparesis sparing the face

Unilateral upper cervical cord lesionsUnilateral upper cervical cord lesions

Brown-Sequard syndrome


IV. Spastic quadriparesis

Lower brainstem lesionsLower brainstem lesions

Lower cranial nerve palsies depending on the site of the lesion

High cervical cord lesionsHigh cervical cord lesions

No cranial nerve deficits Loss of sensory modalities below the site of the

lesion

V. Spastic Paraparesis

Thoracic cord lesionsThoracic cord lesions

Loss of all sensory modalities below the level of the lesion

VI. Spastic monoparesis

Unilateral thoracic cord lesionUnilateral thoracic cord lesion

Brown-Sequard syndrome at the thoracic level

Pattern of LMN weaknessPattern of LMN weakness

I.I. Anterior Horn Cell diseasesAnterior 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)

II.II. Radiculopathy (root lesions) and Plexopathy (plexus lesions)Radiculopathy (root lesions) and Plexopathy (plexus lesions)

- a root lesion will cause muscle weakness in the correspondingmyotome

- if the dorsal roots are also involved, there will be accompanyingsensory loss in defined dermatomal distribution

- a plexus lesion will cause weakness in muscles innervated by- a plexus lesion will cause weakness in muscles innervated bya number of nerve roots which comprise the plexusa number of nerve roots which comprise the plexus

- accompanying sensory loss over several dermatomes may- accompanying sensory loss over several dermatomes maybe presentbe present


II.II. Radiculopathy and PlexopathyRadiculopathy and Plexopathy

Examples of Plexopathies

Brachial Plexus1. Erb’s palsy (C5-6)

- upper plexus injury (loss of shoulder abduction and elbowflexion

2. Klumpke’s palsy (C8-T1)- lower plexus injury (loss of function of the intrinsic musclesof the hand and long flexors and extensors of the fingers)

3. Thoracic outlet syndrome- the brachial plexus and the subclavian artery are compressedby fibrous band or a cervical rib

4. Neuralgic amyotrophy- acute brachial plexus neuropathy which may follow infections, vaccination, or surgery; accompanied by severe pain


II.II. Radiculopathy and PlexopathyRadiculopathy and Plexopathy

Lumbosacral Plexus

Lesions in the lumbosacral plexus includes:

trauma following abdominal surgery or pelvic surgeryneoplastic infiltrationgranulomatous lesionscompression due to aortic aneurysm


III. Disorders of the peripheral nervesIII. Disorders of the peripheral nerves

1. Mononeuropathy1. Mononeuropathy

- disease of a single peripheral nerve eg. Carpal Tunnel syndrome

2. Multifocal neuropathy (Mononeuropathy multiplex)2. Multifocal neuropathy (Mononeuropathy multiplex)

- many single peripheral nerves are involvedeg. Diabetic neuropathy, Sarcoidosis, Leprosy

3. Polyneuropathy (Peripheral neuropathy)3. Polyneuropathy (Peripheral neuropathy)

- more widespread involvement of the peripheral nerves- typically in a symmetric distal distribution

eg. GBS, Vit B12 deficiency


IV. Disorders of the neuromuscularIV. Disorders of the neuromuscularjunction (NMJ)junction (NMJ)

Myasthenia gravisMyasthenia gravisLambert-Eaton Myasthenic SyndromeLambert-Eaton Myasthenic SyndromeBotulismBotulismDrug-induced NMJ malfunctionDrug-induced NMJ malfunction

- the weakness predominantly affects the proximal muscles- the weakness predominantly affects the proximal muscles- may be become widespread in advanced stages- may be become widespread in advanced stages

- in myasthenia, ocular muscles are characteristically affected- in myasthenia, ocular muscles are characteristically affected

- the outstanding feature: easily fatiguable muscles- the outstanding feature: easily fatiguable muscles- wasting is relatively uncommon; reflexes are frequently normal- wasting is relatively uncommon; reflexes are frequently normal


V. Disorders of musclesV. Disorders of muscles

- in myopathies, limb weakness is bilateral and proximal in the - in myopathies, limb weakness is bilateral and proximal in the upper and/or lower limbsupper and/or lower limbs

- muscle wasting may be severe and is restricted to the weak muscle- muscle wasting may be severe and is restricted to the weak musclegroupsgroups

- tone is reduced and is proportional to the muscle wasting- tone is reduced and is proportional to the muscle wasting

Examples of Myopathies:Examples of Myopathies:Progressive Muscular Dystrophies (Duchenne)Progressive Muscular Dystrophies (Duchenne)Inflammatory Myopathies (Polymyositis)Inflammatory Myopathies (Polymyositis)

Disorders of Gait

When assessing gait, the ff. categories should be kept in mind:

Cerebellar ataxiaCerebellar ataxiaSpastic GaitSpastic Gait

Parkinsonian gaitParkinsonian gaitSteppage agitSteppage agitMyopathic gaitMyopathic gait

Apraxic gaitApraxic gaitHysterical gaitHysterical gait

The character of the gait will provide clues to the clinical signs that mightBe expected on further neurological evaluation

Gait of cerebellar ataxia

• patient stands and walks on a wide-based gait (the feet spaced widelypatient stands and walks on a wide-based gait (the feet spaced widelyapart)apart)

• the gait is unsteady, with irregularity of stridethe gait is unsteady, with irregularity of stride• the trunk sways and the patient may veer towards one sidethe trunk sways and the patient may veer towards one side

• in mild cases, the only manifestation of gait disturbance may bein mild cases, the only manifestation of gait disturbance may bedifficulty walking heel-toe in a straight linedifficulty walking heel-toe in a straight line

• always look for cerebellar signs in the limbs; ataxia of gait may bealways look for cerebellar signs in the limbs; ataxia of gait may bethe only sign of cerebellar dysfunction (midline cerebellarthe only sign of cerebellar dysfunction (midline cerebellarlesionslesions

Causes of cerebellar ataxia:Causes of cerebellar ataxia:Multiple SclerosisMultiple SclerosisAlcoholic Cerebellar DegenerationAlcoholic Cerebellar DegenerationAnticonvulsant therapyAnticonvulsant therapyPosterior Fossa TumorsPosterior Fossa TumorsCerebellar Paraneoplastic SyndromesCerebellar Paraneoplastic SyndromesHereditary Cerebellar AtaxiasHereditary Cerebellar Ataxias

Hemiparetic Gait

- there is a characteristic posture on one side (flexion of the upper limb andthere is a characteristic posture on one side (flexion of the upper limb andextension on the lower limbextension on the lower limb

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

Causes:Causes:Cerebral hemispheric stroke syndromesCerebral hemispheric stroke syndromesInfiltrating neoplasms (Glioblastoma multiforme)Infiltrating neoplasms (Glioblastoma multiforme)Traumatic Head InjuryTraumatic Head Injury

Spastic Gait

- seen in patients who have spastic paraparesis or bilateral hemiplegiaseen in patients who have spastic paraparesis or bilateral hemiplegia

- the legs move slowly and stiffly, the thighs are strongly adducted suchthe legs move slowly and stiffly, the thighs are strongly adducted suchthat the legs may cross as the patient walks (scissor gait)that the legs may cross as the patient walks (scissor gait)

Causes include:Causes include:

Spinal Cord diseases / compressionSpinal Cord diseases / compressionSpinal trauma or surgerySpinal trauma or surgeryBirth injuries or congenital deformities (eg CerebralBirth injuries or congenital deformities (eg Cerebral

Palsy, Spina bifida)Palsy, Spina bifida)Multiple Sclerosis (MS)Multiple Sclerosis (MS)Motor neuron Diseases (eg ALS, Primary lateral Sclerosis)Motor neuron Diseases (eg ALS, Primary lateral Sclerosis)Parasaggital meningiomasParasaggital meningiomasSubacute Combined Degeneration of the CordSubacute Combined Degeneration of the Cord

Parkinsonian Gait

• stooped posture and loss of arm swingstooped posture and loss of arm swing

• steps are short and the shufflingsteps are short and the shuffling(festinating gait)(festinating gait)

• there may be difficulty starting, stopping,there may be difficulty starting, stopping,and turningand turning

• having started walking, patient leanshaving started walking, patient leansforward and the paceforward and the pacequickens, as though the quickens, as though the patient has to catch up on patient has to catch up on himselfhimself

Gait of Sensory Ataxia

• due to impaired proprioception by lesions involving the peripheral nerves,due to impaired proprioception by lesions involving the peripheral nerves,posterior root, dorsal columns of the spinal cord, or the ascendingposterior root, dorsal columns of the spinal cord, or the ascendingfibers to the parietal lobesfibers to the parietal lobes

• the gait is “stamping” (shoe soles are equally worn out)the gait is “stamping” (shoe soles are equally worn out)

Causes include:Causes include:Posterior Spinal Cord lesionsPosterior Spinal Cord lesionsVit. B12 deficiencyVit. B12 deficiencyTabes dorsalisTabes dorsalisCervical SpondylosisCervical SpondylosisMSMS

Sensory Peripheral Neuropathies include:Sensory Peripheral Neuropathies include:HereditaryHereditary - Charcot-Marie-Tooth disease- Charcot-Marie-Tooth diseaseMetabolicMetabolic - Diabetic Neuropathy- Diabetic NeuropathyInflammatoryInflammatory - GBS- GBSMalignancyMalignancy - paraneoplstic Syndrome- paraneoplstic SyndromeToxicToxic - alcohol, drugs- alcohol, drugs

Steppage Gait

• arises from weakness of the pretibial and peroneal muscles of thearises from weakness of the pretibial and peroneal muscles of theLMN-typeLMN-type

• patient has “footdrop” and is unable to dorsiflex and evert the footpatient has “footdrop” and is unable to dorsiflex and evert the foot

• the leg is lifted high on walking so that the toes clear the groundthe 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 theon striking the floor, there is “slapping” noise (shoe soles are worn in theanterior and lateral aspects)anterior and lateral aspects)

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

Myopathic Gait

• waddling gait; due to weakness of the proximal muscles of the lower limbwaddling gait; due to weakness of the proximal muscles of the lower limbgirdlegirdle

• the weight is alternately placed on each leg, with the opposite hip andthe weight is alternately placed on each leg, with the opposite hip andone side of the trunk tilting up towards the weight-bearing side,one side of the trunk tilting up towards the weight-bearing side,the weak gluteal muscles cannot stabilize the weight-bearing hipthe weak gluteal muscles cannot stabilize the weight-bearing hip

Causes:Causes:

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

Apraxic gait

• Walks with feet placed apart, and with small, hesitant stepsWalks with feet placed apart, and with small, hesitant steps

• “ “walking on ice”walking on ice”

• there is difficulty initiation of walking, and with advances cases, as if thethere is difficulty initiation of walking, and with advances cases, as if thethe patient is stuck to the floorthe patient is stuck to the floor

• due to frontal lobe disease; look for primitive frontal reflexesdue to frontal lobe disease; look for primitive frontal reflexes

Causes:Causes:Bilateral subcortical strokeBilateral subcortical strokeNormal-pressure hydrocephalusNormal-pressure hydrocephalusAlzheimer diseasesAlzheimer diseasesFrontal Subdural hematomaFrontal Subdural hematomaFrontal lobe tumorsFrontal lobe tumors

Antalgic gait

• arises from pain (painful hip or knee) due to arthritisarises from pain (painful hip or knee) due to arthritis

•Patient tend to weight-bear mainly on the affected sidePatient tend to weight-bear mainly on the affected side

• tendency to hobbletendency to hobble

Hysterical gait

• does not conform to any of the mentioned abnormal gaitdoes not conform to any of the mentioned abnormal gait

• may take a number of forms and is variable in charactermay take a number of forms and is variable in character

• no abnormal formal neurological deficitsno abnormal formal neurological deficits

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Headache ppt