Red Flag Headache - Part 2 PDF

Red Flag Headache – part 2 Chandra Ricks Employability skills developed and enhanced within the clinical neurology module Practice and Problem Solving Communication Patient...

Red Flag Headache – part 2 Chandra Ricks Employability skills developed and enhanced within the clinical neurology module Practice and Problem Solving Communication Patient Awareness Team Working Professional Knowledge/Skills Year 3 CLINICAL NEUROLOGY 2 Lecture outcomes Understand causes and hallmark symptoms and signs of raised ICP Understand common conditions leading to raised ICP and their presentation Understand principles of intracranial tumour – with pituitary adenoma and acoustic neuroma clinical examples Understand principles of brain infection – with meningitis and abscess clinical examples Year 3 CLINICAL NEUROLOGY 3 Space occupying lesion  Blanket term for a mass within a specific area  In the brain could be: ◦ Tumour/Cyst ◦ Aneurysm ◦ Abscess ◦ Other  Not always “malignant” but compression onto brain structure leads to neurological deficit  Also leads to raised intracranial pressure (ICP) What is ICP?  Cranium is an enclosed space  Divided into 3 physiological “compartments” ◦ Cerebral parenchyma - 80% ◦ CSF – 10% ◦ Blood – 10% What is ICP?  ICP is interaction between brain, CSF and cerebral blood  Regulated by: ◦ Cerebral blood flow  Cerebral blood volume/amount is always constant ◦ CSF displacement into the lumbar cistern (enlargement of subarachnoid space)  Normal effectors ◦ Positional changes (standing, decubitus) ◦ Systemic arterial pressure ◦ Valsalva type manoeuvres Normal effectors to ICP 1. Positional changes (standing vs decubitus) 2. Systemic arterial pressure 3. Breathing / Valsalva manoeuvres ◦ Increase intrathoracic pressure (coughing) ◦ Increase intra-abdominal pressure (defecating) ◦ Consequently increase pressure in the jugular veins and/or epidural venous plexus. ◦ Cerebral veins have no valves so increased venous pressure is transmitted to the intracranial space = ↑ICP. Pathophysiology of raised ICP  If “Growth” occurs → fourth compartment created (tumour or haematoma)  Prolonged or severe changes ◦ 1/+ other compartments must become smaller to avoid ↑ICP ◦ In slow-growing lesion, parenchyma deforms or remodels to compensate ◦ Shift of brain structures (herniation)  Many symptoms of raised ICP due to herniation rather than absolute level of ICP Brain Herniations Hallmark symptoms of raised ICP Regardless of cause: Headache often described as throbbing or bursting Aggravated by Valsalva type (strain/sneeze/cough) Aggravated prolonged supine/prone position as gravity doesn’t help to “pull” CSF out Typically pain worse in the morning, ease in day May report new, pulsatile tinnitus aggravated by bending over or being supine May report visual changes – blurring, double vision or “greying out” of vision Nausea – vomiting a later feature Hallmark Testing for raised ICP Physical exam: Valsalva manoeuvre – may aggravate headache Neurological exam CN II – look for blurring or double vision Cranial n. III – pupillary dilation/ptosis CN VI – double vision Other neurological signs – depending on area of compression EG mental status, balance Papilledema – refer out to optician for fundoscopy as this is gold standard for raised ICP Raised ICP Diagnosis CSF pressure monitoring CT scan – bleed MRI - tumour Management Refer immediately! Medically Rx depends on cause Surgery, shunts, pharmaceuticals (diuretics…) hypothermia Benign intracranial hypertension  Definition: raised intracranial pressure of idiopathic origin  Who - Young, obese women  Symptoms = raised ICP headache ◦ Expect brief visual changes (“greying out” with positional change) ◦ Expect “whooshing sound” in ears synchronous with heartbeat or on recumbence  Management – refer immediately (risk of partial blindness)  Treatment – remove CSF, diuretics, weight loss Arterial hypertension headache  Definition: Secondary headache results from rise in arterial blood pressure  Not linked to mild-moderate elevations  Typically caused by very high BP values or very quick rises in BP ◦ Requires urgent referral and medical care:  Hypertensive crisis – acute and severe elevation in blood pressure often described as SBP > 180 mmHg, or DBP > 120 mmHg  Pre-eclampsia or eclampsia  Pregnancy related pathological hypertension Intracranial tumours  Primary tumours originate from neural elements within the brain ◦ Primary tumours incidence 6 per 100,000  Secondary tumours represent spread of distant cancers (metastasis).  Gliomas, metastases, meningiomas, pituitary adenomas and acoustic neuromas account for 95% of all brain tumours.  Benign tumours – SOL, may widely infiltrate brain tissue Intracranial tumours – general principles  Headache ◦ Headache is diffuse but may be unilateral ◦ Slowly progressive over weeks/months  Occasionally acute if start to compress blood vessels or occur in posterior fossa  As tumour progresses develops ICP symptoms ◦ Worse in AM, prolonged supine, agg. Valsalva  May cause neurological symptoms but will be focal to area of compression  Often have seizure involvement Intracranial tumours broadly classified by location approximate to tentorium cerebelli (dura mater extension) Tumours of posterior fossa  More common in children  Origin of 54% and 70% of all childhood brain tumours  Hydrocephalus occurs in 71%-90% paeds pts with PF tumours MRI indicating both PF tumour & hydrocephalus Hydrocephalus Intracranial tumours  Insidious onset of non-  Growth over decades specific headache  Slowly progressive loss of ◦ Raised ICP symptoms hearing and dizziness ◦ Hx of repetitive labyrinthitis  Visual changes over years ◦ Loss of visual acuity  Diffuse occipital ◦ tunnel vision headache  Ptosis and diplopia ◦ Raised ICP pattern  Endocrine dysfunction  May compress ◦ Acromegaly or giantism cerebellum  May compress pons (CN5 ◦ Cushing’s ◦ See review slides for clinical presentation and CN7 possible) Pituitary adenoma Acoustic neuroma (supratentorial) (Infratentorial) Tumour Physical Exam  Test Valsalva manoeuvres for headache agg.  Observe for nystagmus/ptosis  Cranial nerves ◦ Focus: CN2, CN3/4/6, CN8, CN12 ◦ Abnormal pupillary light response  Balance  Cerebellum  Other depending on area suspected of compression Brain Infection  Variable, but most common categories: 1. Meningitis – viral or bacterial infections  Viral less serious, bacterial can be very serious  Meningitis = inflammation – can be related to other causes such as bleeding into the brain 2. Encephalitis  May result from herpes zoster virus, cytomegalovirus or other 3. Abscess  pus-filled “sore” resulting from bacterial infection  Ear infection, chronic sinusitis, mastoiditis, head trauma, surgical procedure… 4. Other – often secondary to: mumps, measles, rubella, AIDs, TB, Lymes disease… Hallmark Signs of Brain Infection  Onset usually over hours – 2 days  Headache ◦ Progressive in severity ◦ Constant  Fever – likely, may be high  Neck stiffness – indicative of meningitis  Photophobia  Fatigue/lethargy  Neurological signs ◦ General – altered mental consciousness, irritability /behavioural changes, ◦ Abscess – focal neuro signs based on location  EG: weakness on ½ body, speech disturbances ◦ Seizure Meningitis  Inflammation of the meninges  Typically caused by 1. Bacterial – rare, but life threatening 2. Viral – more common, often self-limiting 7-10 days  Still needs referral to be seen by medic due to possibility of complications!  Other causes: 3. Blood collection around meninges  EG Subarachnoid haemorrhage 4. Infection – e.g. abscess or encephalitis Meningitis  Classic, hallmark symptoms: ◦ fever, headache, stiff neck or altered mental status  May only have 2 of 4 present  Rash – bacterial meningitis – but VERY LATE SIGN ◦ Do NOT exclude just because it isn’t present  Other possible symptoms: ◦ nausea, vomiting ◦ photophobia ◦ sleepiness, confusion, irritability, delirium, and coma ◦ Bacterial – may have a recent Hx of sinusitis or otitis ◦ Viral – recent Hx of malaise including muscle pain, fatigue, appetite suppression for a couple of days prior Meningitis - Physical Exam  Temperature  Check mental status – may be slight irritability ranging to confusion  Palpate for nuchal rigidity  Reduced neck flexion - aggravates the headache  Bruzinski +ve for pain increase  Kernig +ve for pain decrease (after Bruzkinski) ◦ Bruzinski/Kernig not very sensitive – don’t rely on them to exclude  May see ICP signs – neuro tests for CN2, 3/4/6  Observe for non-blanching rash (late sign) Intracranial abscess  Source of infection ◦ Haematogenous ◦ chronic otitis media/mastoiditis ◦ dental/sinus infection ◦ skull fracture  Presentation ◦ Develops over 2-3 weeks ◦ Pyrexia, malaise ◦ raised ICP headache, ◦ Meningitis symptoms ◦ focal damage Background information for your own review Acromegaly  Acromegaly ◦ caused by growth hormone (GH) hypersecretion in adults  If GH hypersecretion before puberty = gigantism ◦ Results from pituitary tumour  usually a macroadenoma Acromegaly/Gigantism Acromegaly - Symptoms  Hallmark symptoms ◦ General increase in body size ◦ Enlargement of the hands and feet ◦ Enlargement of the bony skull structures: supraorbital ridges and lower jaw ◦ Enlargement of soft tissue in face: lips/tongue/nose ◦ Headache – typically diffuse, progressive  Due to pituitary adenoma typically ◦ Increased sweating Acromegaly - Clinical Features Cushing’s Syndrome  Caused by excessive activation of glucocorticoid receptors→ elevated cortisol ◦ Most common – iatrogenic  prolonged use of synthetic glucocorticoids (prednisolone) ◦ Endogenous uncommon, resulting from:  Adrenal or pituitary tumour  Ectopic ACTH production by other tumours (eg lung)  Pseudo-Cushings: ◦ Cortisol excess from: other illness, alcohol excess, obesity, major depressive illness  4:1 F:M prevalence Cushing’s Syndrome  Hallmark symptoms ◦ Truncal obesity with stria ◦ Buffalo hump ◦ Moon facies ◦ Muscle wasting in extremities (leg focus) ◦ Proximal muscle weakness ◦ Easy bruising and poor wound healing ◦ Depression and mood swings ◦ *headache – diffuse and progressive if caused by pituitary adenoma  Cushing’s Proximal muscle weakness Cushing's syndrome. (A) Clinical features common to all causes. (B) A patient with Cushing's disease before treatment. (C) The same patient 1 year after the successful removal of an ACTH-secreting pituitary microadenoma Cushing’s – Clinical Features Moon Facies References  Mollan SP, et al. (2014) A practical approach to, diagnosis,assessment and management of idiopathic intracranial hypertension. Pract Neurology. 0:1–11.  Rodríguez-Botoa, G., Rivero-Garvíab, M., Gutiérrez-Gonzálezc, R., Márquez-Rivasb J. (2015) Basic concepts about brain pathophysiology and intracranial pressure monitoring. Neurología. 30(1):16—22