40

 

Headache

 

Headache Red Flags

  • Present on  waking
  • Worse on  coughing or bending over
  • Localised
  • Sudden onset
  • Associated with other symptoms:
  • visual, especially in elderly
  • nausea
  • weakness
  • numbness, pins and needles
  • inco-ordination

 

Tension headache
Tight band-like headache encircling the head with tense scalp neck and shoulder girdle muscles.

  • Causes
  • stress and fatigue
  • menstruation
  • loud noises, crowds, bright lights
  • underlying medical conditions eg hypertension,  glaucoma

Chronic Tension headache >15 days /m.

 

Analgesic headache
Due to regular use/overuse  > 15 days per month over last 3 months of simple analgesics NSAIDS opiates and triptans.Often worse first thing in the morning and exacerbated by exercise.Symptoms resolve after withdrawal (cold turkey or gradual tapering)
Medication Overuse Headache DTB 2010;48:2

 

Exercise headache

 

Ice pick headache

 

Migraine
Migraines and cluster headaches are benign vascular headaches involving the constriction and dilation of intra cranial arteriesClassic migraine starts with an aura (migraine with aura) – usually visual (zig zags of light) but sometimes involve visual or speech disturbances, strange smell, and flashes of lights.The aura may occur in isolation but is usually followed within an hour by a severe abrupt onset throbbing unilateral headache which later becomes more generalized and may be incapacitating for hours. Nausea, vomiting,sensitivity to light, and noise is often present.The migraine may be triggered by cheese alcohol OCP periods caffeine anxiety and travel in 50% of patients.Migraines can also occur without the preceding aura (common migraine).

 

Cluster Headache
Excrutiating sudden onset headache typically occurring daily in the early hours of the morning more frequently in males occurring in clusters lasting 6-8 weeksRare more common in smokers. The most common type of cluster headache is the episodic type, in which extremely intense, strictly unilateral pain develops around one eye, often at night; attacks can come on daily or even several times a day, and last for 30 minutes to 2 hours. There is often associated lacrimation of the affected eye, which may be reddened; and nasal symptoms, such as blocked nose. Ptosis may also be present. These episodes can occur at regular intervals for a period of 6-12 weeks at a time, typicallyonce every year or 2 years, often at the same time of year for many years or even decades.There is a chronic form of cluster headache, in which there is no remission of pain between the clusters of headache, and a continuous milder background headache can develop that is present in-between attacks. Verapamil is often used as prophylaxis for patients with cluster headache and triptans may be helpful during an acute attack.

 

 

 

Migraine diagnosis (BASH)

At least five episodes of a headache lasting 4-72 hours, with at least of two of the following four features:

  • 1 Unilateral
  • 2 Pulsating quality (varies with the heartbeat)
  • 3 Moderate or severe intensity of pain
  • 4 Aggravated by exercise.

In addition, the patient must experience nausea/vomiting and/or photophobia/phonophobia during the attack.

Auras typically occur 5-50 minutes before the headache and are visual, consisting of transient hemianopic disturbance or a spreading scotoma. There may also be focal neurological symptoms. Patients with prolonged auras should be referred for further investigation.

 

Migraine treatments
Simple analgesia  eg soluble ibuprofen (400-600 mg), aspirin (600-900 mg) or paracetamol.  taken analgesia asap after symptoms start
Nausea  If the patient complains of nausea, a prokinetic anti-emetic such as prochlorperazine (3 mg buccal tablet), domperidone (20 mg) or metoclopramide (10 mg) can be added; these help by increasing gastric emptying
Rectal analgesia Rectal administration of diclofenac (100 mg) and domperidone (30 mg) may be more effective than oral medication; this should be tried as a second-line therapy.
Triptans If these measures fail, consider a triptan. Patients respond differently to the various triptans on offer, and if there is no response with the first one tried, it is worth changing formulation (eg to a nasal spray) or trying another triptan.Patients should be advised to take the triptan as soon as possible after the headache symptoms start but not until then, ie not during the aura. For all triptans except zolmitriptan, another dose should not be taken for the same migraine. If the migraine recurs however, then another dose can be taken, after an interval of at least 2 hours.If an oral triptan is prescribed, a concomitant anti-emetic should be considered.Oral sumatriptan at a dose of 50 mg is often used as a first choice. The nasal spray offers no real advantage over oral medication if vomiting is a problem, as absorption will still be reduced. Sumatriptan also comes as a subcutaneous injection; this is particularly useful if a rapid effect is required.Other appropriate choices include zolmitriptan 2.5 mg, either as a tablet or as Zomig Rapimelt®, an orodispersible tablet that is placed on the tongue and allowed to disperse, then swallowed. Zolmitriptan is licensed for adolescents.Rizatriptan, 10-mg tablets or wafers, is useful if stronger treatment is required. Rizatriptan interacts with propranolol and in this case the dose should be reduced to 5 mg.Almotriptan and eletriptan are still being evaluated in terms of their exact role in migraine management. Frovatriptan is the longest acting triptan on the market. Naratriptan has a relatively low efficacy and is most useful for patients who have significant adverse reactions to other triptans and in patients with frequent relapses.Some patients find it beneficial to be given more than one type of triptan; for example, sumatriptan tablets and a zolmitriptan nasal spray. That way, if the tablet does not work for a particular migraine, the nasal spray can be tried.

 

Migraine  prophylaxis
If the patient is getting frequent migraines that have an adverse effect on their lifestyle (eg more than four per month), it is then reasonable to considerprescribing a regular prophylactic medication for a period of about 4-6 months. The prophylactic medication can then be slowly tapered off over 2-3 weeks.Beta-blockers such as propranolol or atenolol are usually the first choice unless there is a specific contraindication. The patient commonly starts with a very low dose of beta-blocker, eg 10 mg bd of propranolol, and then gradually has it titrated upwards until it has the desired effect. If one betablocker does not work, it is worth trying another. The patient should take the drug at an optimum dose for 1 month before treatment failure can be established. It is probably preferable to choose a relatively cardioselective beta-blocker initially, to minimise side-effects (eg atenolol 25 mg bd).Amitriptyline 10-150 mg nocte is particularly useful when the migraine coexists with tension-type headaches, chronic pain conditions or insomnia.Again start at a low dose and  titrate upwards.Amitriptyline does not have a licence for migraine prophylaxis.Valproate 300-1000 mg bd is sometimes used as a second-line prophylactic treatment, but is contraindicated in pregnancy or when pregnancy is a possibility. Again, it is not licensed for migraine prophylaxis.Pizotifen is also sometimes used, usually starting at a dose of 0.5 mg taken at night (it has a sedative action). Weight gain and increased appetite are common side-effects. It can be increased in increments of 0.5 mg every week until the patient is on 1.5 mg. Evidence for its efficacy is lacking, however, and it should not be used as a first-line treatment.Verapamil is particularly good as prophylaxis for cluster headaches.Feverfew is an option for patients who want to try a herbal alternative; it can be used at doses of 50-143 mg per day in adults. The primary care migraine guidelines (available at www.eguidelines.co.uk) state that herbal remedies should not be used alone, but only to complement conventional treatment.If these measures do not work, there are other possibilities such as methysergide, which is highly effective but is associated with serious side-effects, including retroperitoneal fibrosis; for this reason, it should be initiated by a specialist.

 

Menstrual migraine
Attacks of migraine (without aura) that occur regularly around the onset of menstruation and at no other time. It is worth suggestinga trial of an NSAID at regular intervals for the duration of the menstrual period (eg mefenamic acid 500 mg tds-qds). Other options are estradiol gel (1.5 mg in 2.5 g) applied daily from day 3 for 7 days (no added progestogens are needed if the woman has regular cycles), the COCP or cerazette® (to inhibit ovulation). These measures should be tried for at least three cycles

 

Idiopathic intracranial hypertension

 

Hypertension and Pregnancy
Conditions of pregnancy such as pre-eclampsia and eclampsia  may also cause severe headaches. Additional symptoms to look for with pre-eclampsia or eclampsia arerapid weight gain, oedema, and hypertension.  If this is left untreated, it can lead to toxemia of pregnancy with development of seizures, hypertensive crisis, or fetal and or maternal death.

 

Temporal arteritis (neurology)
  • severe headache and temporal artery/scalp tenderness assoc with fatigue jaw claudication
  • malaiselwgrade fever lethargy low mood
  • subacute onset over weeks.
  • Risk of sudden blindness.
  • May be assoc with Polymyalgia Rheumatica – morning pain and stiffness in shoulder and pelvic girdle

Rx Prednisolone 40-60mg/day stat. Maintainance 7.5-10mg/day. May need 1-2 years.

 

Infections
Life threatening -meningitis, encephalitis or brain abscess.Headaches are also common complaint associated with everyday infections

 

Meningitis
Caused by bacterial, viral or fungal infection, blood or tumour iniltration.Cardinal symptoms are fever, headache , photophobia, neck stiffness. Papilloedema is a late sign.

 

Encephalitis
 inflammation of the brain itself. Presents with headache preceded by odd behaviour and fits prior to collapse. May be viral esp HSV

 

Head Injury
Consider in all patients presenting with severe headaches and or neurological changes following a recent history of trauma.
 SubduralCollection of blood between brain surface (arachnoid membrane) and the dura due to tearing of the bridging veins particularly in rapid acceleration/decelleration injuries.

  • Acute 72 h  – younger patients high impact injury
  • subacute 3-20 days – headache worsening after recent injury
  • chronic >21 days – elderly patients alcoholics- headache confusion gait disturbance, focal signs seizures

 

 

SAH
  • Arterial bleed into subarachnoid space most often from rupture of cerebral aneurysm at circle of Willis.
  • Associations:hypertension, smoking, alcohol, PCOD, CTD eg Marfans
  • Sudden onset (thunderclap) worst headache ever headache.
  • Menigeal irritation and signs of meningitis.
  • Local vasopasm may also cause focal neurological or cranial nerve signs
  • Raised Intracranial Pressure
  • Confusion, loss of conciousness
 http://www.bbc.co.uk/news/uk-england-17368824

 

CVA and TIA
amaurosis fugax transient loss of vision “like a curtain coming down” due to embolus from internal carotid to opthalmic artery
TIA Focal neurological symptoms lasting <24hrs
Cresendo TIAs Increased in frequency duration and severity of TIAs. Due to critical stenosis pof internal carotid  or carotid dissection.
Stroke  Rapid non-transient neurological deficit from cerebrovascular injury.Focal or global impairement of CNs function developing rapidly and lasting >24hrs.
see also in CVS

 

Carotid artery Disease

Atheromatous plaque at common carotid bifurcation or its branches.  Causes stroke or blindness by thrombosis,  reduced flow or embolisation.

 Stroke Acute Management 

 

FAST  stroke recognition
Face Has their face fallen on one side? Can they smile?
Arms Can they raise both arms and keep them there?
Speech Is their speech slurred? Ask patient to repeat a sentence
Time to call 999 if you see any single one of these signs.

 

Cincinnati prehospial stroke scale
Facial Droop Ask patient to smile
Arm Drift ask patient to close eyes and hold out both for 10 secs
Speech Ask patient to repeat ” The sky is blue over Cincinnati

 

Stroke ABCD2
Age > 60 1 point
BP > 140 systolic or > 90 diastolic 1 point
Clinical Features

  • unilateral weakness – 2 points
  • speech disturbance only – 1 point
  • other/none – 0 points
Duration of symptoms

  • > 60 minutes – 2 points
  • 10 – 59 minutes  – 1  points
  • <10 minutes – 0 points
Diabetes

  • Yes – 1 point
  • No – 0 points
Risk assessment score for urgency of referral after CVA/TUIA
Score >4 or 2 or more TIAs in 1w (crescendo TIAs) or on warfarin — patient at high risk of further stroke: refer immediately
Score <4 or presenting >1w after symptoms resolve — patient at low risk of a further stroke — refer within 1w

All patients with TIA should be given aspirin 300mg immediately and then daily until reviewed in TIA clinic. Normally the dose is stepped down to 75mg after two weeks. Secondary prevention medications are started prior to discharge. Don’t forget they should not drive in the first month – see DVLA guidance.

 

Stroke Classification by pathology
Ischaemic (85%)
  • atherosclerotic thrombosis –  penetrating vessels (lacunar infarcts 25%) larger vessels (eg MCA 20%)
  • cardiac or carotid  emboli 20%
  • cryptogenic 30%
  • others (prothrombotic states, carotid artery dissection) 5%
Haemorrhagic (15%)
  • SAH
  • intraparenchymal

 

Stroke classification by location
Site Signs & Symptoms
Anterior Cerebral Artery lower limb weakness (motor cortex) confusion (frontal lobe)
MCA facial weakness and hemiparesis, hemisensory loss, apraxia, neglect, dysphasia, quadrantopia
Posterior Cerebral Artery Hemianopia
Internal Carotid Artery
Vertebral/Basilar Artery Cranial nerve pathologies + LOC

 

Stroke syndromes territory supplied by clinical syndrome
total anterior circulation infarction TACI middle cerebral artery MCA  
partial anterior circulation infarction PACI branches of MCA or isolated anterior cerebral artery occlusion  
posterior circulation infarction POCI infarction of brainstem cerebellum or occipital lobe
lacunar infarct LACI occlusion of basal perforating arteries

 

Hemiplegia

 

Stroke primary prevention
Lifestyle factors  Healthy diet, alcohol, exercise and smoking cessation advice and treatment.
BP Maintaining a normal BP.
Lipids If CVD> 20% consider a statin using a ‘fire and forget’ approach (Simvastatin 40mg od)If known IHD then lipid management decreases the risk of stoke (Audit standard Cholesterol < 5.0 and LDL < 2.5 BUT aspirational target = Cholesterol < 4.0 and LDL < 2.0). ‘Treat to target’ as per hyperlipidaemia guidelines.
ACE  n known IHD, Peripheral Vascular Disease (PVD) or DM with 1 risk factor e.g. smoking or dyslipidaemia in patients aged over 55 then consider using a Ramipril starter regime and aim to work the dose up to10mg a day.
Anticoagulants Antiplatelets  All patients with valvular heart disease and AF should be considered for warfarin. Only use the CHAD score to determine anticoagulation use in patients with non valvular AF.

 

Stroke secondary prevention
Lifestyle factors Healthy diet, alcohol, exercise and smoking cessation advice and treatment.Annual  review should check BMI, smoking status/cessation advice, alcohol intake, BP and bloods
BP BP should be maintained at <130/<80 (unless they have bilateral coronary artery stenosis). The audit standard is <150/<90.
Anticoagulants Antiplatelets Aspirin – all patients with a history of ischaemic stroke should be on low dose aspirin, as this reduces CVS mortality and recurrent stroke.Patient’s with TIA or stroke benefit from Aspirin & Dipyridamole for 2 years and then revert to aspirin alone – Esprit study.
Statins All patients with a history of ischaemic stroke irrespective of age, sex or cholesterol level should commence a statin to achieve a minimum audit standard of Cholesterol < 5.0 and LDL < 2.5 BUT the aspirational target = Cholesterol < 4.0 and LDL < 2.0mmol/l. Start with an adequate dose e.g. Simvastatin 40mg. Warn the patient about common side or serious side effects e.g. myalgia. Check fasting lipids and ALT at 4 weeks. Uptitrate the dose if not at target (e.g. Simvatsatin 40, then Simvastatin 80, then Atorvastatin 40mg) and repeat lipids in another 4 weeks. Once at target they only need annual review.
ACEI  ACE inhibitors Ramipril 10 mg a day in stoke patients > 55 years decreases CVD deaths and recurrent stroke – HOPE trial.
Endarterectomy All patients with non disabling stroke or TIA should be considered for urgent specialist assessment – patients with high grade ipsilateral stenosis benefit from carotid endarterectomy.
almost all ischaemic stroke and TIA survivors should be taking low dose aspirin, an ACE inhibitor, another antihypertensive and a statinAlmost all stroke/TIA patients will benefit from treatment statins and blood pressure medication regardless of actual levels plus aspirin + AF (source Red House Bradford?)

 

 

UMN LMN UMN LMN
Power reduced reduced
Tone increased – spastic paralysis decreased – flaccid paralysis
Wasting only if lack of use prolonged yes
Reflexes increased decreased or absent
Clonus yes no
Plantars extensor flexor

 

Aphasias
Broca’s / Expressive motor association cortex of frontal lobe good non-fluent dysarthric agrammatical
Wernicke’s / Receptive posterior temporal lobe poor fluent grammatical meaningless
Conduction arcuate fasciculus good fluent grammatical
Global substantial language area poor very little

 

Broca’s  BROKen aphasia-broken speech
Wernicke’s  Wordy  aphasia- wordy, but making no sense

 

Dysarthrias and  Speech Disorders
Staccato speech cerebellar disease
Scanning speech combination of cerebellar and pyramidal disease eg MS or phenytoin overdose

EEP Infopoems Aug 2011 Screening tool for dysphagia after stroke

 

Bulbar palsy pseudubulbar palsy
Bulbar palsy
  •  is a LMN lesion of CN 9/10/12 due to MND MS  or sryngobulbia
  • bilat tongue wasting + fasiculations palatal paralysis dysarthria and (rarely) extraocular palsy.
Pseudobulbar palsy
  •  due to bilateral UMN lesions –  CVA . Causes donald duck speech and emotional lability.
  • Causes spastic paralysis of tongue amd patate with dysarthria and emotional lability.

 

Brainstem lesions

Top Of Midbrain

Pontomedullary Junction

Lateral medullary lesions

 

Weakness and Clumsiness

 

Ataxia
Clumsy uncoordinarted movements due to poor postural control due to to cerebellar or sensory nerve (posterior column) disease.
Gait ataxia incoordination when walking
Cerebellar ataxia Patients with cerebellar lesions fall to the side of the lesion – if asked to walk in circles will walk in ever decreasing or ever increasing circles.
Truncal  ataxia tendancy to fall backwards whilst sitting or standing – suggests midline cerebellar lesions.
Friedericks ataxia  AD spinocerebellar disorder presenting in childhood or adolescence. Associated with pes cavus, pes equinovarus, and kyphoscoliosis.
Ataxia telangiectasia  rare inherited disorder with nystagmus, conjunctival and skin telangiectasia.

 

Posterior Column Dysfunction

 

Rombergs Sign
  • Sign of posterior column disease. (Patients can mitigate against sensory (but not cerebellar) ataxia using visual clues.
  • Patient stands with feet together and closes eyes
  • Sign is positive if  patient sways so much with eyes closed they would fall if otherwise unsupported.
youtu.be/fNasho7u0hM

 

 

Gait Abnormalities

Gait Analysis

 

 

Tremor inc Benign Essential
Physiological  “physiological” –  fine tremor.  Similar tremor found in anxiety, hyperthyroidism and alcoholism.
Benign essential  Sightly larger amplitude. More common in elderly. Worse on movementRelieved by alcohol and by propranolol (eg 10-40 mg bd) often bilateral.
Parkinsonian  Coarse (4-7 Hz) resting  pill-rolling tremor   –  unaffected by alcohol or betablockers -usually unilateral onset
Intention  increases in amplitude as the hand reaches the target – with overshooting/past-pointing – demonstrated by finger-nose and nose-examiner’s finger testing –  suggests cerebellar disease.
Titubation  vertical nodding  tremor of head when sitting or standing  in some patients with cerebellar disease especially patients with MS
Flapping  asterixis – liver failure, Wenickes encephalopathy, uraemia, hypercapnia, CCF. Denonstrated with arms outstretched and hands dorsiflexed
Hysterical
neurology.org Oct 2011 Tremor

 

Bells Palsy
idiopathic isolated LMN lesion of the facial nerve
Solitary, unilateral facial nerve paralysis (including forehead) causing drooping of the mouth, loss of nasolabial fold loss of forehead furrowing and difficulty closing eyes smiling blowing out cheeks an whistlingA lower motor neurone lesion causes weakness of all the muscles of facial expression. The angle of the mouth falls. Weakness of frontalis occurs, and eye closure is weak.Associated symptoms—Patients with Bell’s palsy commonly feel pain in or behind the ear. Numbness can occur on the affected side of the face. Loss of taste on the ipsilateral anterior two thirds of the tongue is common. Hyperacusis due to stapedius paralysisBells phenomenon – eyeball rols up but lids remain open when attempting to close the eye.
CVA
CVA causes UMN and sparing the upper half of the face – blinking, eye closure and frontalis not affected – patients would usually have ipsilatera hemiparesis +/- speech difficultiesWith an upper motor neurone lesion frontalis is spared, normal furrowing of the brow is preserved, and eye closure and blinking are not affected.Check that no other cranial nerves are involved.
Treatment
Oral prednisolone and aciclovir in patients with moderate to severe palsy, ideally within 72 hours but up to seven days from onset of symptoms. Prednisolone should be prescribed at a dosage of 1 mg/kg/day (maximum 80 mg daily) for the first week, with the dosage tapering off over the second week. Exclude R_H first (see below)Aciclovir may be given (800 mg five times a day for five days)Eye protection – taping, protective glasses, artificial tears.
Prognosis
90% recover within 2-12w. Aberrrant reinnervation may occur.

 

Causes of facial nerve palsy
Bell’s palsy idiopathic LMN facial nerve palsy – diagnosis of exclusion. Normal looking ear. Pure tone audiogram is required. Acycolvir 400mg + steroids 60mg OD for 5 days. Pts reviewed in clinic after one week. Eye protection at night.
Ramsey-Hunt Rapid onset, pain, vesicles in ear canal, pinna + sometimes soft palate If it involves 8th nerve ?Hearing loss +vertigoLook also for a painful rash over the ear, which indicates Ramsay Hunt syndrome caused by herpes zoster virus.and any presence of rash that may indicate herpes zoster.
Supporative OM Distinguish  from serous otitismedia by the presence of purulent fluid in the middle ear.IV abx + nasal decongestants. No clinical improvement after 24-48 hrs emergency myringotomy
Nerve compression  2ndry to compression or dehiscence of nerve
Trauma Palsy present in 20% of longitudinal + 80% transverse temporal bone fractures. Look for CSF otorrhoea or rhinorrhoea. Ix: Fine cut axial CT scan
other DD otitis-mastoiditis,  multiple sclerosis, trauma, parotid tumor, acoustic neuroma sarcoidosis (may cause bilateral LMN lesion) Lyme disease

 

Facial Nerve Palsy -House-Brackmann grading
Grade1 Normal
Grade2 Slight weakness, good eye closure with minimal effort
Grade3 Obvious weakness, complete eye closure, strong but asymmetrical mouth
Grade4
Grade5 Motion barely perceptible, incomplete eye closure, slight movement of corner of mouth
Grade6 No movement

 

Cranial Nerve Palsies

http://hacking-medschool.com/cranial-nerves

 

 

Horners
  • Partial ptosis
  • Small pupil with loss of direct light reflex
  • Enopthalmos
  • Anhydrosis (decreased sweating) on that side of the face
Causes

  • Brainstem lesion causing autonomic paralysis
  • C8/T1 lesions eg sryngomyelia, sryngobulbia
  • Superior mediastinal lesions – Pancoast tumour, aneurism, glandular enlargement
  • Neck lesions – trauma, lymphadenopathy
(see also Opthalmology for these sections below)

 

 

Ptosis
Drooping of upper eylelid which normally covers only 1/6 of the cornea.may be unilateral or bilateral, partial or complete with or without overaction of frontalisCauses

  • muscular ( MG, dystrophica myotonica, fascioscapulohumerol myopathy)
  • neurological (eg Horners, 3dd nerve lesions, tabes dorsalis)

 

 

Oculomotor palsies

 

 

CN 3 palsy
  • Eyeball externally rotated ( due to unopposed action of lateral rectus)
  • Ptosis (paralysis of levator palpebris,
  • Dilted pupil (unopposed action of sympathetic nerves) with loss of light and accomodation reflex
Causes

  • Vascular – thrombosis, posterior communicating artery aneurism, haemorrhage
  • Neoplasm
  • DM
  • MS
youtu.be/fMAIYqPNiYY

 

 

CN 4 palsy

 

 

CN 6 palsy
Paralysis of lateral rectus hence medial deviation of affected eye (convergent squint) due to unopposed action of medial rectus with diplopia  inability to move laterally on testing.
Causes

  • Raised ICP – due to stretching of the nerve (false localising sign)
  • Vascular  – internal carotid aneurism
  • Neoplasm
  • Encephalitis
  • MS
youtu.be/3M1GhgV8px0

 

 

Cerebellar dysfunction
  • Cerebellar signs DANISH
  • dysdiadochokinesis
  • ataxia
  • nystagmus
  • intention tremor (approx 3hz)
  • scanning/staccato speech
  • hypotonia
Tests of cerebellar function

  • Heel to shin – get patiennt to run right heel slowly and accurately up left shin from ankle to knee then vice-versa.
  • Finger to nose
  • Finger to finger (Drs)
  • Rapid alternating movements – diysdiadochocinesia – get patient to tap one hand (+/- foot)  rapidly on the back of the other and vice versa – and /or rapidly pronate/supinate hand at the wrist.
  • In cerebellar disease patient’s writing tends to become larger and more untidy ( cf micrographism of Parkinsons disease)

 

 

Cerebellar tumours

 

 

Posterior fossa lesions

 

CNS infections (neurology)

 

Meningitis (neurology)

 

Encephalitis

Inflammation of brain substance, most commonly due to viral infection (HSV, HZ, mumps…).

Meningitis like picture +/- drowsiness/behavioural changes/confusion/seizures.

 

 

Fits faints funny turns blackouts

Dizzyness & Vertigo see ENT

Syncope see Cardiology

  • Syncope = transient LOC with loss of postural tone
  • Mechanical fall = coming to land on the ground with no LOC

 

Epilepsy
Seizure = paroxysmal synchronised cortical electrical discharge.

 

Siezure Types
Partial – localised

  • temporal lobe
  • frontal lobe
  • occipital
Simple Partial – does not affect conciousness
Complex Partial – affects conciousness
Generalised

  • tonic clonic
  • abscence attacks
  • myoclonic
  • atonic (drop attacks)
  • tonic
Abscence (petit mal)
Clonic
Tonic
Tonic Clonic(grand mal, major motor)
Atonic
Akinetic
Febrile
Status Epilepticus

 

Focal Seizures
Frontal lobe Motor Seizures Motor convulsions
Jacksonian March
Todds paralysis
TLE aura and hallucinations
Frontal Lobe complex partial seizure LOC automatisms rapid recovery
Rapid Medicine Sam & Teo W-B

 

Generalised Seizures
Tonic ClonicGrand Mal aura– generalised spasm (tonic) –repetitive synchronous jerks (clonic) +/- incontinence tongue biting — post ictal
Absencepetit mal LOC but upright posture maintained– staring into space blinkingor other repetitive movement –immediate recovery
Non convulsive status epilepticus Acute confusional state
Rapid Medicine Sam & Teo W-B

 

Patients with suspected epilepsy should be referred to a specialist as soon as possible, ideally within 2 weeks (NICE 2004).

Treatment  is generally recommended after a second seizure. However, it may be instigated by a specialist after the first seizure if the patient has a neurological deficit, the EEG shows definite epileptic activity, brain imaging is abnormal, or if the patient is unable to accept the possibility that they may experience a second seizure.

 

Epilepsy and QOF

hacking-medschool/qof/epilepsy

 

Epilepsy Rx

 

Monitoring epilepsy Rx

Blood levels are only necessary in the following circumstances:

To determine compliance with treatment

If there is suspected toxicity

If the dose of phenytoin needs to be adjusted

If there is concern about interaction with other medications

New-onset liver or kidney failure.

NICE recommends that all patients on enzyme-inducing drugs (carbamazepine, topiramate, oxcarbazepine, phenytoin and phenobarbital) should have routine bloods done every 2-5 years, including full blood count (FBC), urea and electrolytes (U&Es), liver function tests (LFTs), vitamin B12 levels and calcium.

 

Stopping Epilepsy Rx

The longer a patient has been seizure-free on treatment, the better their prognosis.

The following factors increase the risk of relapse on withdrawal of medication:

  • Age of onset of epilepsy >16 years
  • Being on more than one anti-epileptic medication
  • History of seizures while taking medication
  • History of tonic-clonic or myoclonic seizures
  • Abnormal EEG.

After 5 years of being seizure-free, a patient with one or two of the above risk factors has approximately a 20-30% risk of recurrent seizures on withdrawal of the medication (compared to a 10-15% risk if they continue taking it).

After 10 years of being seizure-free, this risk drops to about 10% (or 5% if they continue taking the medication). The risk of a recurrent seizure is highest 9 months after withdrawal of treatment.

Anti-epileptic medication needs to be tapered off gradually over 2-3 months, usually under the supervision of a specialist. Only one medication should be stopped at a time.

 

Epilepsy and contraception

Epilepsy.org.uk/info/women

superceded by the above guidelines

For women taking hepatic enzyme-inducing anti-epileptic drugs – carbamazepine, topiramate, oxcarbazepine, phenytoin and phenobarbital:

The progesterone-only pill is not recommended.

The progesterone implant is not recommended either.

If the combined oral contraceptive pill is used, at a minimum initial dose of 50 micrograms. oestrogen is recommended. ‘Tricycling’ might be necessary if the woman experiences breakthrough bleeding.

If the depot progesterone method is preferred, injections need to be given at intervals of 10 weeks instead of 12 weeks.

Women on anti-epileptic drugs should be advised that the doses of levonorgestrel used for emergency contraception need to be increased to 1.5 mg and 750 micrograms taken 12 hours apart.

 

Parkinson’s disease
Common neurological disease of older people due to progressive degeneration of dopaminergic neurones axon terminals of cells projecting from substantia nigra to caudate nucleus and putamen (extrapyramidal system)Prevalence 160/100 000, 2% over 80s, annual incidence 13/100 000 total numbers 100 000
Presents with

  • 1 tremor
  • 2 rigidity (often ‘cogwheel’)
  • 3 bradykinesia (and difficulty in stopping or starting walking)
  • 4 loss of postural reflexes causing instability

Slowness and poverty of emotional and voluntary movement, rigidity and tremor.

Early signs are loss of facial expression (mask-like facies) , general ‘slowing down’ of movements and unilateral loss of arm swing. Fatiguing occurs with repetitive movements such as opening and closing the hand, pronating and supinating the wrist or tapping the heel on the ground.
  • Pill rolling tremor
  • Akinesia
  • Rigidity
  • Kyphosis
  • Instability
  • Neck Stiffness
  • Shuffling gait (becomes festinant when patient pushed)
  • Oculogyric Crises
  • Nose (glabellar) tap – on repeated tapping of the glabellar the patient continues blinking
Presents with

  • 1 tremor
  • 2 rigidity (often ‘cogwheel’)
  • 3 bradykinesia (and difficulty in stopping or starting walking)
  • 4 loss of postural reflexes causing instability

Slowness and poverty of emotional and voluntary movement, rigidity and tremor.

Early signs are loss of facial expression (mask-like facies) , general ‘slowing down’ of movements and unilateral loss of arm swing. Fatiguing occurs with repetitive movements such as opening and closing the hand, pronating and supinating the wrist or tapping the heel on the ground.

 

Parkinsons syndrome (Parkinsonism)
  • iatrogenic (treatment with dopamine antagonists eg phenothiazine neuroleptics)
  • cerebrovascular disease (often sudden onset) and arteriosclerosis
  • postencephalitic
  • toxic (Wilsons disease/CU, Mn, CO)

 

Parkinsons guidelines ***
Goal of therapy is to reduce symptoms, functional impairment and effect on patients lifeTreatment considerations are complex and therapy should be initiated or altered by a SpecialistTherapy is usually initiated with ldopa, monoamine oxidase type-B inhibitors, selegiline or dopamine agonists.Excessive daytime sleepiness and sudden onset of sleep can occur with levodopa and dopamine receptor agonists.Patients starting treatment with these drugs should be warned of the possibility of these effects.Patients who have suffered excessive sedation or sudden onset of sleep, should refrain from driving or operating machines until these effects have stopped recurring.Warned patients about the potential for dopamine agonists, and less commonly levodopa to cause impulse control disorders such as pathological gambling, binge eating and hypersexuality.

Older patients are more susceptible to adverse drug effects and treatment should be initiated at low doses and increased with caution.
l-dopa carbidoparelieves symptoms in most patients, but long-term use is associated with motor complications such as involuntary movements (dyskinesia), as well as a shortened response to each dose (wearing-off phenomenon) and unpredictable ‘on-off’ fluctuations.
L-dopa plus dopa decarboxolase inhibitor l-dopa carbidoparisk of motor side effects over time
L-dopa plus dopa decarboxolase inhibitor l-dopa carbidoparisk of motor side effects over time
Dopamine agonists
  • ropinerole
  • pramipexole
  • pergolide

monotherapy or adjuncts to l-dopa

less likely to cause dyskinesia

first-line in younger patients without serious co-morbidities
MAOI B inhibitors selegilineUsing a dopamine agonist or selegiline initially may reduce the need for ldopa
COMT inhibitors entacapone

 

L-dopa preparations
Initiate at low dose and increase gradually to minimise side effects. Adjust Dosage, timing and frequency to suit individual patient needs
Co-beneldopa Madopar
Name levodopa benserazide carbidopa
Madopar 62.5 50mg 12.5mg –
Madopar 125 100mg 25mg –
Madopar 250 200mg 50mg –
Madopar dispersible 62.5 50mg 12.5mg –
Madopar dispersible 125 100mg 25mg –
Madopar CR 125 100mg 25mg –
Co-careldopa Sinemet
Name levodopa benserazide carbidopa
Sinemet 62.5 50mg – 12.5mg
Sinemet 110 tabsCo-careldopa 10/100 100mg – 10mg
Sinemet Plus Co-careldopa 25/100 100mg – 25mg
Sinemet 275Co-careldopa 25/250 250mg – 25mg
Half Sinemet CR 100mg – 25mg
Sinemet CR 200mg – 50mg

 

Drugs and doses
Co-beneldopa (Madopar®)Dose: Expressed as levodopa, initially 50mg 3-4 times daily, increase by 100mg once or twice weekly according to response; usual maintenance dose 400 – 800mg daily in divided doses after meals. Elderly: initially 50mg once or twice daily, increased by 50mg daily every 3-4 days according to response.
Co-careldopa (Sinemet®)Dose: Expressed as levodopa, initially 100mg 3 times daily, increased by 50-100mg daily or on alternate days according to response, up to 800mg daily in divided doses after food.
Note: Please refer to BNF for advice on dosage when transferring patients from immediate-release levodopa preparations to modified release preparations.The total daily dose of carbidopa should be at least 70mg. A lower dose may not achieve full inhibition of peripheral dopa-decarboxylase, resulting in an increase in adverse effects.Nausea and vomiting due to co-beneldopa or co-careldopa may be reduced by taking doses after food. Vomiting can be controlled with domperidone in a dose of 10-20mg three times daily, see section 4.6. Levodopa should not be withdrawn abruptly. Patients should be warned that levodopa might colour urine dark red.Dispersible co-benelopa may be useful for patients with swallowing difficulties or where rapid absorption is desired, for example first thing in the morning. Modified release preparations are not recommended for initiation of therapy, they may help with ‘end-of- dose’ deterioration or nocturnal immobility and rigidity.
Dopamine receptor agonistsDopamine receptor agonists may be considered for patients with early Parkinson’s disease and motor symptoms or for the management of complications in patients with advanced Parkinson’s disease, either used alone or as an adjunct to levodopa with dopa-decarboxylase inhibitor.
ROPINIROLE or PRAMIPEXOLERopinirole (as hydrochloride) tablets 250micrograms, 500micrograms, 1mg, 2mg, 5mg; 28-day starter pack of 42x250microgram (white) tablets, 42x500microgram (yellow) tablets, 21x1mg (green) tablets; 28-day follow-on pack of 42x500microgram (yellow) tablets, 42x1mg (green) tablets, 63x2mg (pink) tabletsDose: Initially 750micrograms daily in 3 divided doses, increased by increments of 750micrograms at weekly intervals to 3mg daily; further increased by increments of up to 3mg at weekly intervals according to response; usual range 9-16mg daily; maximum 24mg daily. Note – when administered as an adjunct to levodopa, concurrent dose of levodopa may be reduced by approx. 20%.Prolonged release ropinirole tablets (Requip® XL ?) are only licensed for patients with established adequate symptomatic control on immediate release (standard) ropinirole, they may be prescribed under the direction of a specialist. Substitution of ropinirole prolonged release tablets for ropinirole immediate release tablets should be supervised by an appropriate specialist in Parkinson’s disease.Pramipexole tablets 88micrograms, 180micrograms, 350micrograms, 700microgramsNote: Doses and strengths are stated in terms of pramipexole (base); equivalent strengths in terms of pramipexole dihydrochloride monohydrate (salt) are as follows:88micrograms base ? 125micrograms salt; 180micrograms base ? 250micrograms salt; 350micrograms base ? 500micrograms salt; 700micrograms base ? 1mg saltDose: Initially 88micrograms 3 times daily, dose doubled every 5-7 days if tolerated to 350micrograms 3 times daily; further increased if necessary by 180micrograms 3 times daily at weekly intervals; maximum 3.3mg daily in 3 divided doses.Prolonged release pramipexole tablets (Mirapexin® Prolonged Release) may be prescribed under the direction of a specialist in patients for whom the use of pramipexole is appropriate, to provide the benefit of once daily dosing at an equivalent cost.Rotigotine transdermal patch (Neupro® ?) may be prescribed under the direction of the Neurology Clinic or Geriatric Medicine for either advanced Parkinson’s disease in combination with levodopa, when transdermal administration would facilitate treatment or for early stage idiopathic Parkinson’s disease as monotherapy in patients with swallowing difficulties or poor compliance. Patches require storage in a refrigerator.Dopamine receptor agonists may cause nausea and vomiting; patients can be treated with domperidone at a dose of 10-20mg three times daily, see section 4.6.Dopamine receptor agonists are associated with more neuropsychiatric side effects than levodopa and can cause hypotensive reactions and postural hypotension. When used as adjunctive therapy, dopamine receptor agonists can exacerbate levodopa-induced adverse effects.Ergot-derived dopamine receptor agonists, bromocriptine, cabergoline, and pergolide, have been associated with pulmonary, retroperitoneal, and pericardial fibrotic reactions and require regular clinical monitoring. See MHRA Drug Safety Update, October 2008 for further information. They should not be used as first line treatment for Parkinson’s disease and are only initiated on specialist advice.
Monoamine-oxidase-B inhibitors
Selegiline hydrochloride tablets 5mg, 10mg, liquid 10mg/5mL, oral lyophilisates (freeze-dried tablets) 1.25mg (Zelapar®)Dose: Conventional tablet/liquid, 10mg in the morning or 5mg at breakfast and midday. Zelapar®, initially 1.25mg daily before tablet should be placed on the tongue and allowed to dissolve.Selegiline, a monoamine-oxidase-B inhibitor, may be used in advanced Parkinson’s disease in conjunction with levodopa to reduce ‘end-of-dose’ deterioration. Patients with early Parkinson’s disease and motor symptoms may also be considered for treatment. In trials of patients with early Parkinson’s disease early treatment with selegiline delayed the need for levodopa therapy. Selegiline also has a levodopa sparing effect when given simultaneously with levodopa associated with a reduction in motor fluctuations but not dyskinesias. Selegiline oral lyophilisates (Zelapar®) is a buccal formulation that avoids first-pass metabolism. It may be considered in patients unable to tolerate the conventional tablets.
Catechol-0-methyltransferase inhibitors
Entacapone tablets 200mgDose: 200mg with each dose of levodopa with dopa-decarboxylase inhibitor; maximum dose 2g daily.Entacapone, a catechol-O-methyltransferase inhibitor, may be used in advanced Parkinson’s disease in conjunction with levodopa to reduce ‘end-of-dose’ deterioration. For patients stabilized on co-careldopa and entacapone, a combination product, Stalevo® may be suitable.

 

Co-careldopa with entacapone Stalevo
Max 10 tablets daily (7 for Stavelo 200/50/200)1 tablet to be taken for each dose, to limit the amount of entacapone taken
Stavelo levodopa carbidopa entacapone
50/12.5/200 50mg 12.5mg 200mg
75/18.75/200 75mg 18.75mg 200mg
100/25/200 100mg 25mg 200mg
125/31.25/200 125mg 31.25mg 200mg
Stalevo150/37.5/200 150mg 37.5mg 200mg
200/50/200 200mg 50mg 200mg

 

Antimuscarinic drugs
used for extra-pyramidal side effects not be used as first line treatmentless effective than dopaminergic drugs and associated with neuropsychiatric and cognitive adverse effects. They should therefore not be given to patients with comorbidities such as cognitive impairment or significant psychiatric illness. They should also be avoided in older patients due to their adverse effects. Abrupt withdrawal of antimuscarinics should be avoided.
Procyclidine or orphenadrine may occasionally be useful in patients with tremor unresponsive to other drugs, on the advice of a specialist. They may also reduce Parkinsonian symptoms induced by antipsychotic drugs.in patients with Parkinson’s disease as they are

 

Restless leg syndrome
  • Restless legs syndrome URGE
  • is there an Urge to move the legs?
  • does Resting bring it on?
  • does Getting up and moving about help?
  • Are Evenings worse?

 

 

Cramps

 

Multiple sclerosis MS
Episodic autoimmune inflammatory disorder affecting myelinated nerves (white matter) within the brain and spinal cord and leading to scarring (sclerosis).Usually starts in early adulthood. Attacks/ lesions are disseminated in time and place.
Relapsing/remitting MSSymptoms come and go. Periods of good health or remission are followed by sudden symptoms or relapses (80% of people at onset)
Secondary progressive MSFollows on from relapsing/remitting MS. There are gradually more or worsening symptoms with fewer remissions (about 50% of those with relapsing/remitting MS develop secondary progressive MS during the first 10 years of their illness)
Primary progressive MSFrom the beginning, symptoms gradually develop and worsen over time (10–15% of people at onset)Between three and seven people per 100 000 population are diagnosed with MS each year and about 100 to 120 people per 100 000 population have MS. From these rates it is estimated that in England and Wales about 1800 to 3400 people are newly diagnosed with MS each year and that 52 000 to 62 000 people have MS

 

Motor neurone disease MND
  • Progressive degenerative disease with destruction  of motor neurones in spinal cord cranial nerves and cortex.
  • AMLS
  • Fasiculations – spontaneous twitching of individual motor units.

 

Chorea
  • Huntingtons
  • Rheumatic
  • Pregnancy
  • Senile
  • Wilsons disease

 

Huntingtons chorea
AD degenerative disease of Basal gangia causing progressive dementia with abnormal quasi-purpuseful rapid jerking movements affecting face tongue and distal extremities.

 

Hemiballismus
Involuntary one sided  rapid violent flinging  from full extension to abduction or internal rotation due to lesion of subthalmic nucleus.

 

Myaesthenia Gravis
? neuromuscular junction dysfunction.? tensilon® test: 2mg I.V. ? repeat 4mg X 2 prn ? have atropine ready.Myasthenic crises ? inadequate dose of medication, too much medication, refractory to meds, orinfection/stress/trauma.L ABC’s, atropine prn, Solu-cortef® prn, withhold meds prn until the tensilon® test is positive, and treat theprecipitating cause, e.g. UTI.? unlike myasthenia gravis and botulism, with the Lambert-Eaton syndrome, the hand grip strengthincreases with repetition, the so-called upwards staircase phenomenon (may occur with Ca of the lung).

 

GBS Guillian Barré syndrome
Acute ascending peripheral neuropathy

 

Tick Paralysis

 

Syringomyelia

 

Neurofibromatosis
AD inherited disorder affecting neural crest cells.
Type 1 Von Recklinghausens – spinal and cutaneous neurofibromas

  • Discrete cutaneous fibromas especially on the trunk along the path of peripheral nerves.
  • Cafe au lait spots.
  • Axillary freckling.
  • Kyphoscoliosis.
  • Deafness and cerebellar signs ( acoustic neuroma).
  • Occasionally associated with phaeochromocytoma.
Type 2 Schwanommas

 

Paraesthesia and Numbness

 

Pins and Needles in the Hand

 

Peripheral Neuropathy

Investigating peripheral neuropathy BMJ 2010

  • Peripheral neuropathy ABCDE
  • Alcohol
  • B12
  • CRF and carcinoma
  • Diabetes and drugs
  • Every vasculitis

 

Mononeuritis multiplex
Mononeuritis Multiplex SCALD

  • Sarcoid
  • Ca
  • Arteritis
  • Leprosy
  • Diabetes
4

 

Polyneuropathies

iTunes U Polyneuropathies Rock Valley College

 

Radiculopathy

 

Peripheral nerves

 

Peripheral nerve lesions

 

Ulnar palsy – claw hand

C7/8/T1 supplies

flexor carpi ulnaris – ulnar flexion of hand

flexor digitorum profundus (medial fibres) – flexion of distal phalanx of ring and little fingers

adductor pollicicis – Froments test – weakness  causes flexion of  distal phalanx when attempting to hold onto piece of paper between thumb and clenched fist.

abductor digiti minimi – abduction of little finger

opponens digiti minimi – opposition of little finger

flexor digiti minimi – flexion of little finger –

interossei (dorsal and palmar) and 3rd 4th lumbricals – flexion of prox phalanx, extension of distal and middle phalanx, (P)adduction and  (D)abduction

(ie all the intrinsic muscles of the hand except 3 muscles of the thenar eminence APB OP FPB and the 3rd and 4th lumbricals)

Cutaneous sensation to ulnar border of hand on dorsal and palmar aspects, little finger and ulnar half of ring finger

May be damaged by fractures around the elbow or lacerations to forearm or wrist.Ulnar lesion below elbow produces clawing of 4th and 5th fingers (due to overextension of  MCPs and flexion of the IPs due to unopposed action of long flexors an extensors) with slight separation of ring and little fingers and wasting of small muscles.

Causes

Injury/tethering around olecranon groove.

If bilateral – sryngomyelia, MND, cervical spondylosis, cervical cord tumours

 

Wrist Drop – Radial Nerve

C5  6 7 8 supplies

Triceps and anconues  – forearm extension

Brachioradialis – forearm flexion

Extensor Carpiradialis – radial extension of hand

Extensor digitorum – extension of phlanges of all 4 fingers

Extensor digiti minimi – extension of phlanges of little finger

Extensor carpi ulnaris – unar extension of hand

Supinator – supination of forearm

Abductor pollicis longus – abduction of metacarpal of thumb

Extensor pollicis brevis – extension of thumb

Extensor digitorum longus – extension of index finger

Due to fracture of humerus involving spiral groove.

Lesion causes wrist drop due to weakness of triceps, ECR, ED and EPL. Patient unable to extend the wrist, fingers at MCP joints and the thumb.

Sensory loss to posterior aspect of thumb and dorsoradial side of hand + posterior aspect of forearm in higher lesions

(may in fact be minimal due to overlap from median and ulnar territories)

 

Median Nerve Palsy

C678 T1 supplies

Pronator teres – probation of forearm

Flexor carpi radialis – radial flexion of hand

Palmaris longus – flexion of hand

Flexor digitorum superficialis – flexion of middle phalanx of all 4 fingers

Flexor pollicis longus – flexion of terminal phlanx of thumb

Flexor digitorum profundus – flexion of terminal phalanx of index and middle fingers

Lateral lumbricals  – flexion of prox phalanx and extension of middle and distal phlanges of index and middle finger

Opponens pollicis – opposition of metacarpal of thumb

Abductor pollicis brevis -abduction of metacarpal of thumb – straight raise thumb vertically with back of hand on table.

Flexor pollicis brevis – flexion of proximal phalanx of thumb

Cutanous senstion to volar aspect of thumb, index and middle fingers

Lesions cause wasting of the thenar eminence with thumb falling in a flat simian position

 

Foot drop

Damage to common peroneal or lateral popliteal nerve  where it winds round head of the fibula.

 

Autonomic neuropathy

Autonomic Neuropathy Medscape

 

Myopathies

Myopathies American College of Rheumatology

 

Charcot Marie Tooth CMT HMSN PMA
Relatively common  (1 in 2500) group of inherited  (AD)  neurological disorders affecting mainly  motor (and sensory) peripheral nerves causing causing weakness and atrophy of  peroneal muscles of calf leading to inverted champagne bottle appearance. and small muscles of feet causing claw foot (pes cavus) Due to segmental demyelination of peripheral nerves with associated degeneration of the nerve axons and anterior horn cells.Reflexes are diminished and sensation mildly affected.Pes Cavus = high arched foot = increased height of dorsal longitutudinal arch with dorsal contracture of MTP joints – most commonly occurs in isolation but may be associated with neurological conditions – PMA, Friederichs sryngomyelia spina bifida.aka hereditary motor and sensory neuropathy HMSN or peroneal muscular atrophy PMA
ninds article

 

Myotonic dystrophy
Autosomal dominant. condition presenting in adult life with muscular dystrophy (wasting and weakness) and myotonia (abnormal sustained contraction)Features: wasting of head and neck muscles esp sternal heads of sternomastoid, bilateral ptosis,cataracts, frontal balding, distal muscle weakness especially forearms, testicular atrophy.
Atrophy  AD
Baldness
Cataracts Chromosome 9
Droopy eyes Dysphagia Diabetes
EF expressionless face or forehead – wasting of muscles of facial expression
Gonadal atrophy (small pituitary fossa)
Heart – cardiomyopathy conduction defect
Immunology low serum Ig intellectual deterioration

 

Fascioscapulohumeral dystrophy
  • AD
  • weakness of facial muscles and sternomastoids
  • ptosis
  • winged of scapula,
  • reduced reflexes in affected muscles
  • no sensory involvement
  • Advanced cases may involve  lower limb and pelvic girdle muscles.

 

 

CNS tumours
Meningioma  Commonest
Astrocytoma  Fibrillary  (cerebrum) or pilocytic ( cerebellum and brainstem)
Gioblastoma multiforme  High-grade invasive tumour
Haemangioblastoma  Vascular tumour often in cerebellum
Pituitary adenoma  benign. Space occupying  and endocrine effects
Oligodendroglioma 10% gliomas. Epileptiform.
Medulloblastoma  Invasive midline cerebellar tumour in children
Ependymoma  Bening tumour of spinal cord and 4th ventricle
lymphoma  In immunosuprresed. Highly malignant.

Presentation
Headache, vomitting , fits, peronality changes, focal neurological defects, false localising signs

 

Localising syndromes
Olfactory grove  anosmia frontal lobe dysfunction
Caverous sinus  Squint (CN 3,4,6) V1/V2 sensory loss
Foster Kennedy (sphenoid meningioma)  CN2 compression with ipsilateral optic atropy and papilloedema
Pituitary fossa Bitaemporal hemianopia (optic chiasm compression from suprasellar extension), hypopituitarism or hypersecretion syndromes
Parinaud’s Syndrome (pineal)  Impaired upgaze (superior midbrain lesion) or obstructive hydrocephalus (3rd ventricle)
Parasagittal region Spastic pararparesis mimicking cord compression
Cerebellopontine  Unilateral deafness facial weakness then unilateral ataxia nad hemifacial sensory impairement
 Rapid Medicine Sam & Teo – Wiley Blackwell

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