Summary
Summary Neuro Revision Posters
- Module
- Medicine
- Institution
- The University Of Sheffield (TUOS)
Revision posters for Neurological Diseases
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By: sophiacotterell • 4 year ago
By: physician786 • 6 year ago
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HEADACHESHeadaches can be divided into secondary headache (defined pathophysiological basis) or primary headache (uncertain
pathogenesis; generally more benign, migraine and tension-type headaches, primary headaches more common. Headache
o=en accompanies stroke, esp. when caused by haemorrhage, intracranial venous sinus thrombosis or arterial dissec@on.
Metabolic disturbances e.g. hypoxia, hypercapnia and hypoglycaemia, can trigger headache, as can vasoac@ve drugs and
other substances (E.g. alcohol, monosodium glutamate, nitrites, nitrates).
GIANT CELL ARTERITIS
Disorders of intracranial pressure: Headache due to raised ICP e.g. cerebral trauma: characteris@cally present on waking/ Giant cell arteriAs = important in pt>50y. Granulomatous inflammato
may wake pt at night. May improve later in day. Some@mes, occipital ‘burs@ng’ pain. May be exacerbated by sneezing, branches of external caro@d artery, esp superficial temporal vessels,
straining, bending, li=ing, lying down: all may raised ICP further. to the op@c nerve head. Blood vessels show narrowing of lumen, -ma
Headache caused by intracranial tumour generally short history (days, weeks, months). Usually a crescendo quality: pain uncertain: viral infxn and autoimmunity have been implicated.
becomes increasingly severe and persistent, ul@mately occurring daily. May be associated N&V. Effortless N&V = symptom Usually present with headache, may be non-specific but may localize
of a mass in posterior fossa, close to 4th Ventricle, irrita@ng the vomi@ng centre tenderness when comb hair. Pain on chewing due to impaired blood
Headaches may also signify low ICP: hallmarks = rela@on to posture – pain rapidly relieved upon lying down. Spontaneous claudica@on of jaw). Temporal arteries may become swollen and non
low-pressure headache = increasingly recognized phenomenon. Transient loss of vision in one eye (amourosis fugax) = ominous symp
complete blindness. Diplopia may result from CN3 or CN6 involveme
Idiopathic (‘benign’) intracranial hypertension: typically young obese women.S&S of raised ICP, but no mass lesion Cons@tu@onal symptoms: low grade fever, night sweats, shoulder an
iden@fied on cranial imaging with CT or MR. Pathophysiology = incompletely understood; may involve impaired CSF weight loss.
absorp@on. Present with morning headache, vomi@ng and some@mes visual disturbance (diplopia and visual obscura@ons More generalized arteri@s includes disturbance of liver func@on, rare
[sudden, transient bilateral visual loss with changes in posture]). Tinnitus = also common symptom. of intracranial vessels, i.e. stroke, esp in vertebrobasilar territory.
Examina@on reveals bilateral papilloedema. Unilateral or bilateral CN6 palsies may be present as ‘false localizing sign’ of Threat to vision and neuro consequences, early diagnosis and treatm
raised ICP, but no other focal neuro signs found. Salient inves@ga@ons:
CT scanning of brain excludes mass lesion and reveals ventricles of normal/ small size. CSF examina@on by LP (safe a=er ESR o=en grossly raised (>100mm/h): CRP high
exclude intracranial mass) confirms raised pressure (o=en very high, >40cm of CSF) with normal CSF contents. Condi@on Bloods: normochromic, normocy@c anaemia and abnormal LFTs, esp
may be self-limi@ng, resolving completely with weight loss, and a=er one/ few LPs. In some pa@ents, however, it is more Temporal artery biopsy: Important if posi@ve; but nega@ve biopsy do
chronic; threat to vision from secondary op@c atrophy: in such instances, medical treatment with CA inhibitor not be uniformly involved; may get skip lesions histologically); pa@en
acetazolmamide, other diure@cs (e.g. chlortalidone) or cor@costeroids may be successful. Surgical interven@on may be req Treatment: If giant cell arteri@s is suspected, take bloods (ESR); treat
either to drain CSF via lumboperitoneal shunt or to protect op@c nerve via fenestra@on procedures (op@c nerve sheath biopsy.
incision). Benign intracranial HTN = idiopathic by defini@on, but similar syndrome may be symptoma@c of: Condi@on is highly sensi@ve to cor@costeroids, but high doses (40-60
Intracranial venous sinus thrombosis; Hypervitaminosis A; Disturbances of calcium metabolism; SLE; Drugs, inc Rapid response to steroids is helpful diagnos@cally; pa@ents o=en fee
tetracyclines and cor@costeroids Dose gradually tapered down, according to the pa@ent’s symptoms a
18months-2 years
Meningism (irrita@on of meninges) e.g. by inflammatory processes (like in acute meningi@s) or blood (subarachnoid Urgent treatment: prevent permanent loss of vision.
haemorrhage), characteris@cally severe global/ occipital headache with vomi@ng, exacerba@on of symptoms by bright
lights (photophobia) and neck s@ffness (nuchal rigidity). Allied condi@on =polymyalgia rheuma;c: girdle pains + morning s@ff
In subarachnoid haemorrhage, pain usually very sudden in onset (Seconds) and severe, may lose consciousness. without the cranial manifesta@ons of giant cell arteri@s; is also drama
In bacterial meningi;s, headache acute in onset, but usually worsens over minutes/hours. requiring lower dosage (7.5-15mg daily prednisolone)
Nuchal rigidity: assessed by determining pa@ent’s resistance to passive neck flexion. Meningism may be demonstrated by
Kernig’s sign: pain and resistance to passive knee extension with hip flexed. In some, esp children, nuchal rigidity may be
due to posterior fossa mass rather than diffuse meningeal process, but in such individuals Kernig’s sign is usually nega@ve
MIGRAINE
Cluster headaches: unilateral headache; dis@nct from migraine, but the two condi@ons may coexist. Migraine = periodic disorder; unilateral (some@mes bilateral) headac
Histaminergic and other humoral mechanisms thought to underlie the autonomic accompaniments of headache. Usual visual disturbance. Migraine = common; >10% popula@on experience
pa@ent: male, age of onset 20-60years. Severe afacks of pain around one eye (always same side): typically lasts at any age: typical onset within teens/20s: women>men.
20-120mins; may recur several @mes daily; o=en waken more than once in the night. Alcohol may precipitate an afack.
Majority of pa@ents have posi@ve FH. Many individuals with travel sic
Pafern con@nues for days, weeks, months; pt may then be symptom-free for many weeks, months, years. Pt o=en migraine. Rela@onship to HTN and head injury.
restless during an afack, and may appear red (rather than pale like migraine). Autonomic accompaniments of pain: Underlying pathophysiology obscure, but ini@al neurological symptom
conjunc@val injec@on, lacrima@on and nasal discharge or conges@on. Full-blown Horner’s syndrome may develop and phenomena) tradi@onally afributed to phase of intracerebral vasoco
persist following the afack. All phenomena are unilateral, occurring on side of pain. extracerebral vessels in the scalp and dura) may be responsible for th
Treatment: high-flow100% oxygen, ergotamine, sumatriptan, cor@costeroids (E.g. 2-week reducing course of prednisolone
involvement of 5HT pathways along with vasoac@ve neuropep@des. G
or dexamethasone). migraine have recently indicated a role for calcium channels in the pa
Longer-term preventa@ve treatment: methysergide, verapamil or pizo@fen. Various factors may trigger migraine afacks: stress (esp a=er stress i
Lithium = helpful if clusters become more chronic, but blood levels must be monitored physical exercise; diet (alcohol, occasionally specific diet triggers: che
Several other condi@ons in which unilateral headache and/or facial pain are associated with autonomic features: some of migraine may follow menarche; symptoms may increase around men
these are rare trigeminal-autonomic syndromes are strikingly responsive to indomethacin.
menstrua@on.
Tension headache: Very common condi@on; unknown cause though abnormal contrac@on of muscles of H&N has been Migraine with aura (classical migraine): Vague prodromal symptom
invoked as one mechanism. Muscle contrac@on may be triggered by psychogenic factors, i.e. anxiety/depression, or by drowsiness, mood changes, hunger, anorexia. Classical afack begins
local disease of H&N, e.g. cervical spondylosis or dental malocclusion. Descrip@ons of the headache vary from dull pain at expanding scotomata, which may scin@llate (teichopsia). Crenated or
various sites, to global pressure sensa@on, to feeling of a @ght band around the head. More exo@c and bizarre descrip@ons spectra). Homonymous hemianopia/ complete blindness may result.
may point to a psychogenic basis. No associated symptoms; neuro examina@on is normal. unilateral numbness and paraesthesia may affect the face, arm/leg. D
Migraine and tension-type headache frequently co-exist. generally resolves a=er 15-20minutes (may last up to an hour), at wh
Treatment: reassurance. A 3-6month course of tricyclic or related compound (e.g. amitriptyline or dosulepin) may help if some pa@ents, headache and focal neurological symptoms coexist. H
tension-type headache is frequent or persistent including relaxa@on exercises, or psychotherapy (Stress management). o=en contralateral to side of hemianopia. Pain is throbbing, may be e
(jolt phenomenon). Lasts several hours (4-72 hours). Pa@ents prefer t
Chronic daily headache = headaches on 15+ days/ month sleep. Associated symptoms: photophobia, N&V, pallor and diuresis.
Causes: secondary headache syndromes; chronic tension-type headache; ‘transformed migraine’ (normal migrainous Migraine without aura (common migraine). Aura absent, but pa@en
features may persist whilst normal periodicity of migraine is lost). symptoms. Headache may be present on waking, but otherwise is sim
One major cause = medica@on overuse; pa@ents may inadvertently overuse analgesics, triptans or ergotamine, and Basilar migraine (Bickerstaff variant). Par@cularly affects teenage fem
convert episodic headache syndrome into a chronic problem. Withdrawal of overused medicine can be achieved using of vertebrobasilar ischaemia during aura: ver@go, diplopia, dysarthria
transi@onal strategies to cover the period of withdrawal headache, e.g. with NSAIDs (or steroids), an@-eme@cs and Hemiplegic and ophthalmophlegic migraine: Rare syndromes; migra
dihydroergotamine. or ophthalmoplegia, with focal neurological signs persis@ng for days
Preventa@ve measures should be introduced ASAP (tricyclic and related drugs. structural causes, e.g. aneurysm, have been excluded.
Other causes of headache and facial pain Diagnosis: almost exclusively by history; periodicity of afacks very im
Cough and exer@onal headaches = usually benign; in some pa@ents MRI reveals cerebellar @ssue protruding into the usually las@ng <3 days, then pain-free periods varying from days-mon
foramen magnum (cerebellar ectopia). Con@nuous headache week a=er week = unlikely to be due to straigh
Coital headache – usually benign, but may be severe and sudden enough to warrant inves@ga@on to exclude subarachnoid migrainosus may develop.
haemorrhage. Neuro exam NAD (Except during afack of hemiplegic/ophthalmopleg
‘Ice pick’ headaches = brief, sharp jabs of pain felt anywhere in the head; generally benign infarc@on has occurred) – helps to differen@ate migraine from more
increased ICP.
Rare finding: cranial bruit: alert physician to possibility of migraine b
brain.
FACIAL PAIN DD of transient focal nuerological symptoms: Migraine; Transient cer
Many neurological syndromes (e.g. giant cell arteri@s, cluster headache and migraine) present with facial pain rather than
Migraine can be dis@nguished by rate of spread of symptoms: much s
headache. Other syndromes have pain restricted to the face.
than seconds or less), and by associated symptoms.
Trigeminal neuralgia typically pt>50y; due to compression of trigeminal sensory root adjacent to brainstem; previously
Focal neurological features always recurring on the same side may pr
subdivided – idiopathic vs symptoma@c. Symptoma@c trigeminal neuralgia includes tumours of cerebellopon@ne angle
lesion, but strict unilaterality is much more likely to be due to migrain
and MS (demyelina@on affected trigeminal sensory fibres within the brainstem). Even in idiopathic trigeminal neuralgia,
history than any other cause.
there is an iden@fiable cause of compression of trigeminal sensory root, usually an aberrant arterial loop.
Pa@ents with unilateral facial pain within distribu@on of 1+ divisions of trigeminal nerve (mandibular and maxillary
Management
divisions most commonly affected). Pain is lancina@ng – brief, severe, sharp, stabbing, electric shock-like jolts of pain, may
Lie in darkened room; sleep; Simple soluble analgesics e.g. paracetam
eventually be con@nuous. O=en ‘trigger’ areas,: even gentle pressure may produce pain. Pt may be reluctant to wash
Episodes unresponsive to such measures can be treated with ergotam
faces/shave for fear of provoking an afack. Some@mes speaking/cold breeze is sufficient to cause pain. Chewing food may
sumatriptan (selec@ve 5HT1 receptor agonist; may be given subcutan
be difficult, resul@ng in weight loss.
Ergot alkaloids may cause acute poisoning (ergo@sm) with vomi@ng,
Glossopharyngeal neuralgia = similar (rarer) disorder with pain in throat/deep inside ear. In general, pt with trigeminal
the extremi@es, chest pain, pruri@s and cardiac dysrhythmias. Chroni
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