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neurology Flashcards

1
Q

Ischaemic stroke definition

A
  • Acute neurological deficit lasting more than 24 hours and caused by cerebrovascular aetiology
  • Ischaemic stroke is caused by vascular occlusion or stenosis
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2
Q

how common is Ischaemic stroke

A
  • Third leading cause of death and a major cause of disability in the us
  • Most occur in people over 65
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3
Q

causes of stroke (Ischaemic)

A

• 3 main causes:

  • Primary vascular pathologies: atherosclerosis, aortic arch atherosclerosis, arterial dissection, migraine or vasculitis  directly reduce cerebral perfusion and/or result in artery-to-artery embolism (i.e. stenosis or occlusion of a distal artery by an embolus originating in a proximal artery)
  • Cardiac pathologies: AF, MI, patent foramen ovale  that lead to cerebral arterial occlusion due to embolism
  • Haematological pathologies: prothrombotic hypercoagulable or hyperaggregable states  that directly precipitate cerebrovascular thrombosis (particularly venous) or facilitate systemic venous or intracardiac thrombus formation and cardioemebolism
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4
Q

risk factors for stroke (Ischaemic)

A
  • Older age
  • Fx of stroke or hx of ischaemic stroke
  • Hypertension
  • Smoking
  • Diabetes
  • AF
  • Comorbid cardiac conditions
  • Carotid artery stenosis
  • Sickle cell disease
  • Dyslipidaemia
  • People with lower levels of education
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5
Q

symptoms of ischaemic stroke

A
  • Vision loss or visual field deficit  monocular vision loss may occur and is often transient – common early warning signal for cervical carotid stenosis, bilateral = vertebrobasilar ischamia, unilateral = carotid or vertebrobasilar ischaemia
  • Weakness  complete or partial loss of muscle strength in face, arm and/or leg – weakness of all 3 suggests deep hemispheric involvement, hemiparesis is associated with lacunar strokes
  • Aphasia  impairment in any language function
  • Ataxia  absence of muscle weakness, ataxia points to ischaemia involving the cerebellum or its connections with the rest of the brain
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6
Q

signs of Ischaemic stroke

A
  • Carotid territory symptoms: amaurosis fugax (transient loss of vision, aphasia, hemiparesis, hemisensory loss, hemianopic loss.
  • Vertebrobasilar territory symptoms: diplopia, vertigo, vomiting, choking and dysarthria, ataxia, hemisensory loss, meianopic or bilateral visual loss, tetraparesis, loss of consciousness (rare)
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7
Q

DDx of Ischaemic stroke

A
  • Intracerebral haemorrhage
  • TIA
  • Hypertensive encephalopathy
  • Hypoglycaemia
  • Complicated migraine
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8
Q

Investigations for Ischaemiac stroke

A

• 1st LINE:

  • CT HEAD: to rule out intracranial haemorrhage, hypoattenuation (darkness) of the brain parenchyma, loss of grey matter-white matter differentiation and sulcal effacement; hyperattenuation (brightness) in an artery indicates clot within the vessel lumen
  • MRI BRAIN: acute ischaemic infarct appears bright on diffusion-weighted imaging; at later stages, T2 images may also show increased signal in the ischaemic territory
  • SERUM GLUCOSE AND ELECTROLYTES: may exclude hypo/hyperglycaemia and/or electrolyte disturbance
  • SERUM CREATININE AND UREA: may exclude renal failure
  • CARDIAC ENZYMES: exclude MI
  • ECG: exclude arrhythmia or ischaemia
  • FBC: exclude anaemia and thrombocytopenia
  • PROTHROMBIN TIME AND PTT: may show coagulopathy
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9
Q

management of ischaemic stroke

A

• 1ST LINE:

  • Aspirin: continued long-term, clopidogral can be given instead of aspirin if needed
  • With patients who have carotid artery stenosis  carotid endarterectomy
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10
Q

prognosis and complications of ischaemic stroke

A

prognosis is dependant on cause

complications include aspiration pneumonia, depression and DVT

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11
Q

haemorrhage stroke definition

A
  • Stroke is an acute neurological deficit caused by cerebrovascular aetiology
  • Haemorrhagic stroke is due to rupture of a cerebrospinal artery resulting in intrparenchymal, subarachnoid and intraventricular haemorrhage
  • Intracerebral haemorrhage is further subdivided into primary and secondary aetiology
  • Primary HIS: haemorrhage in the absence of vascular formations or associated diseases
  • Secondary HIS: has an identifiable vascular malformation or as a complication of other medical or as a complication of other medical or neurological diseases that either impair coagulation or promote vascular rupture
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12
Q

how common is haemorrhagic stroke

A
  • Third most common cause of death in the UK
  • Per annum, 110,000 strokes
  • More than 900,000 in England are living with the effects
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13
Q

who does haemorrhagic stroke affect

A

most common in people >65

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14
Q

causes of haemorrhagic stroke

A
  • Intracerebral haemorrhagic stroke: there is bleeding from a blood vessel within the brain. High blood pressure is the biggest cause of this
  • Subarachnoid haemorrhage: Bleeding between the brain and the arachnoid matter.
  • Some experts do not classify a subarachnoid haemorrhage as a stroke as they present differently to ischaemic strokes/intracerebral haemorrhages, and require different treatment.
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15
Q

risk factors for haemorrhagic stroke

A
  • Hypertension
  • Advanced age
  • Male sex
  • Asian, black and/or Hispanic
  • Haemophilia
  • Cerebral amyloid angiopathy
  • Anticoagulation
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16
Q

symptoms/ signs of haemorrhagic stroke

A
  • Neck stiffness
  • Hx of AF or liver disease
  • Visual changes
  • Photophobia
  • Sudden onset
  • Altered sensation
  • Headache
  • Weakness
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17
Q

DDx of haemorrhagic stroke

A
  • Ischaemic stroke
  • Hypertensive encephalopathy
  • Hypoglycaemia
  • Complicated migraine
  • Seizure disorder
  • Conversion and somatisation disorders
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18
Q

investigations for haemorrhagic stroke

A

• 1ST LINE:

  • NON-INFUSED HEAD CT – differentiates haemorrhagic from ischaemic stroke – hyperdense lesion
  • CHEMISTRY PANEL – normal
  • FBC – necessary to exclude thrombocytopenia as a cause of haemorrhage – usually normal
  • CLOTTING TESTS – rules out coagulopathy as a cause of haemorrhage – usually normal
  • ECG – signs of mI, cerebral T waves
  • INTRACEREBRAL HAEMORRHAGE (ICH) SCORE – score for prognosis after early onset of intracerebral haemorrhage
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19
Q

management of haemorrhagic stroke

A

• 1st LINE:

  • Anticoagulant agents should be stopped and effects reversed through prothrombin complex concentrates
  • Pts with a large intracerebral haematoma which is causing a deepening coma, brainstem compression or cerebellar bleed causing hydrocephalus as a result of obstruction of the drainage pathways for CSF should be immediately referred for neurosurgical evaluation
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20
Q

prognosis and complications of haemorrhagic stroke

A

prognosis - higher than ischaemic

complications - delirium, DVT, infection, seizures

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21
Q

TIA definition

A

• Transient episode of neurological dysfunction caused by a focal brain, spinal cord or retinal ischaemia without acute infarction

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22
Q

how common is TIA

A
  • Third most common cause of death in the UK
  • Per annum 20,000 TIAs
  • More than 900,000 in England are living with the effects

most occur in people >65

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23
Q

causes of TIA

A
  • In situ thrombosis of an intracranial artery or artery-to-artery embolism of thrombus asa result of stenosis or unstable atherosclerotic plaque (16%)
  • Cardioembolic events (29%)  intracardiac thrombus may form in response to some secondary risk factor such as staiss from impaired ejection fraction or AF, precipitating factor may be a thrombogenic nidus within the heart such as an infectious vegetation or artificial valve, thrombus can pass from the venous system across a cardiac shunt to create paradoxical emboli
  • Small vessel occlusion (16%) – microatheromas, fibirnoid necrosis and lipohyalinosis of small penetrating vessels are seen
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24
Q

risk factors for TIA

A
  • AF
  • Valvular disease
  • Carotid stenosis
  • CHF
  • Hypertension
  • Diabetes
  • Smoker and alcohol abuse
  • Old
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25
Q

symptoms/signs for TIA

A
  • Report of neurological deficit
  • Bried duration of symptoms
  • History of cardiac disease
  • Unilateral symptoms  TIAs represent ischaemia in an are of brain controlling function on the contralateral side of the body
  • Increased BP on presentation
  • Absence of headache, shaking, scotoma, spasm, migraine, seizure prior to neurological deficit
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26
Q

DDx for TIA

A
  • Hypoglycaemia
  • Seizure with post-seizure (Todd’s) paralysis
  • Complex migraine
  • Conversion disorder
  • MS
  • Peripheral neuropathy
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27
Q

Investigations for TIA

A

• 1st LINE:

  • BLOOD GLUCOSE: hypoglycaemic events can elicit global symptoms such as confusion or syncope, can mimic TIA  blood glucose <3.3 suggests hypoglycaemia as mimic of TIA
  • CHEMISTRY PROFILE: severe hyponatraemia can trigger seizure or induce generalised weakness  very low sodium, potassium or high calcium suggests non-ischaemic cause of symptoms
  • FBC: elevated WBC can suggest infection  usually normal
  • PROTHROMBIN TIME, INR AND ACTIVATED PTT: this is used if the neurological deficit persist at time of presentation, there is reason to suspect abnormal coagulation (liver disease or use of anticoagulant therapy) and thrombolytic therapy for stroke is being considered
  • ECG: evaluate for AF and other arrhythmias  AF may be present
  • BRAIN MRI WITH DIFFUSION: half will have positive diffusion images
  • FASTING LIPID PROFILE: all pts should be treated with statin therapy unless contraindications are present
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28
Q

management of TIA

A

• 1ST LINE:
- ANTIPLATELET THERAPY: aspirin 300mg
o + statin: atorvastatin

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29
Q

prognosis and complications for TIA

A

Prognosis - most significant risk to the pt is a second ischaemic event causing permanent disability

Complications - stroke, MI

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30
Q

Sub-Arachnoid Haemorrhage definition

A

• Bleeding into the subarachnoid space – the area between the arachnoid membrane and the pia mater surrounding the brain

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31
Q

how common is Sub-Arachnoid Haemorrhage

A
  • Accounts for 5% of strokes
  • Incidence of 6 per 100,000 per annum.

• Mean age of presenting pts is 50

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32
Q

causes of Sub-Arachnoid Haemorrhage

A

• Spontaenous arterial bleeding into the subarachnoid space
• Can be caused by:
o Saccular ‘Berry’ Anuerysms (70% of cases)  acquired lesions that are most commonly located at the branching points of the major arteries coursing through the subarachnoid space at the base of the brain (circle of willis)
o Congenital arteriovenous malformations (10%)
o No lesion can be found in 20% of cases

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33
Q

risk factors for Sub-Arachnoid Haemorrhage

A
  • Hypertension
  • Diabetes
  • Anticoagulation
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34
Q

symptoms for Sub-Arachnoid Haemorrhage

A
  • Thunderclap headache (being kicked in the head)  pulsates towards the back of the head
  • Vomiting
  • Seizures
  • Confusion
  • Neck stiffness
  • Hemiparesis (weakness of one side of the body)
  • Head injury
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35
Q

signs for Sub-Arachnoid Haemorrhage

A
  • Signs of meningeal irritation  neck stiffness and positive kernings sign
  • Focal neurological signs
  • Subhyaloid haemorrhages (between the retina and vitreous membrane) with or without papilloedma
  • Warning headache a few days before the bleed
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36
Q

DDx for Sub-Arachnoid Haemorrhage

A
  • Migraine
  • Aneurysm
  • Trauma
  • Seizure
  • Hypoglycaemia
  • Mass lesions
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37
Q

investigations for Sub-Arachnoid Haemorrhage

A

• 1st LINE:
- IMMEDIATE CT: shows subarachnoid or intravascular blood in 95% of cases when the scan is done in 24hrs
o + lumbar puncture indicated if there is a strong clinical suspicion of SAH but the CT scan is normal  increase in pigments (bilirubin and/or oxyhaemoglobin released from lysis and phagocytosis of RBCs) is the key finding to support SAH, must be performed at least 12hrs after onset and can be detected up to 2 weeks after onset
- MR ANGIOGRAPHY: performed to establish the source of bleeding in all pts potentially fit for surgery

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38
Q

prognosis and complications for Sub-Arachnoid Haemorrhage

A

prognosis is poor

complications include re-bleeding

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39
Q

management for Sub-Arachnoid Haemorrhage

A

• 1st LINE:

  • ANTI-HYPERTENSIVES: ramipril or calcium channel blocker (depending on race and if over 55)
  • CALCIUM CHANNEL BLOCKER: nimodipine can be given to reduce cerebral artery spasm
  • SURGERY: obliteration of the aneurysm by surgical clipping or insertion of a fine wire coil under radiological guidance prevents re-bleeding
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40
Q

peripheral neuropathy definition

A

• Lymphadenopathy (swelling) of the cervical lymph nodes (glands in the neck)

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41
Q

how common is peripheral neuropathy

A

• Common presentation in infection and in malignancy

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42
Q

causes of peripheral neuropathy

A
  • 6 principles that cause nerves to malfunction  demyelination, axonal degeneration (due ot a toxin), Wallerian degeneration following nerve section, compression, infarction (in arteritis) and infiltration by inflammatory cells (e.g. sarcoid)
  • MONONEUROPATHY = process affecting a single nerve, may be the result of acute compression particularly where the nerves are exposed anatomically (common peronaeal) or entrapment, particularly where the nerve runs through a relatively narrow anatomical passge (carpal tunnel)
  • MULTIPLE MONO-NEUROPATHY/MONONEURITIS MULTIPLEX = affects several or multiple nerves, often indicates a systemic disorder, treatment is that of the underlying disease, acute presentation is most commonly due to vasculityis when prompt treatment with steroids may prevent irreversible nerve damage
  • POLYNEUROPATHY = acute or chornic, diffuse, usually symmetrical disease, may involve motor, sensory and autonomic nervesm either alone or in combination, sensory symptoms include numbness, tingling ‘pins and needles’, pain in the extremities and unsteadiness on the feet, numbness tends to affect distal arms and legs in a ‘glove and stocking distribution’, motor symptoms are usually those of weakness, autonomic neuropathy causes postural hypotension, urinary retention, erectile dysfunction, diarrhoea, diminished sweating, impaired puoillary response and cardiac arrhythmias, many varities of neuropathy affect autonomic function to some degree, but occasionally autonomic features predominate  occurs in diabetes, amyloidosis and guillian-barre syndrome

• CAUSES: (DAM IT BITCH)
- D Drugs and chemicals (Pb, phenytoin, metronidazole, amiodarone, hydralazine, vincristine, isoniazid, organic solvents, sulphonamides, nitrofurantoin, CO, OPs)
- A alcohol (with or without Thiamine deficiency)
- M metabolic (diabetes, hypoglycaemia, uraemia)
- I infection (HIV, leprosy, lyme, diptheria, syphilis) or post infectious (GBS)
- T tumour (paraneoplastic phenomenon – lung, lymphoma, myeloma)
- B B12 & other vitamin deficiency states, as well as pyridoxine excess
- I idiopathic and infiltrative (e.g. amyloidosis)
- T toxins (botulism, ciguatera, Tetrodotoxin, Saxitoxin, BRO, tick paralysis)
- C connective tissue diseases (e.g. SLE, PAN, RhA) and congenital (e.g. CMT)
H Hypothyroidism

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43
Q

risk factors for peripheral neuropathy

A
  • Diabetes
  • Alcohol abuse
  • Vitamin deficiencies
  • Infections e.g. lyme disease, shingles, Epstein-barr virus, hepatitis B and C
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44
Q

symptoms/signs for peripheral neuropathy

A
  • SENSORY NEUROPATHY: pins and needles in the affected body part, numbness and less ability to feel pain or changes in temperature, particularly in your feet, a burning or sharp pain, usually in the feet, feeling pain from somethingthat should not be painful at all, such as a very light touch, loss of balance or co-ordination caused by less ability to tell the position of the feet or hands
  • MOTOR NEUROPATHY: twitching and muscle cramps, muscle weakness or paralysis affecting one or more muscles, thinning (wasting) of muscles, difficulty lifting up the front part of your foot and toes, particularly noticeable when walking (foot drop)
  • AUTONOMIC NEUROPATHY: constipation or diarrhoea, particularly at night, feling sick, bloating and belching, low BP which can make you feel faint or dizzy when you stand up, rapid HR, excesive sweating, erectile dysfunction, urinary retention, loss of bowel control
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45
Q

DDx for peripheral neuropathy

A
  • Diabetes
  • Trauma
  • MS
  • Cord compression
  • Brain lesion
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46
Q

Investigations for peripheral neuropathy

A

• 1ST LINE:
Bloods - FBC, U&E’s, CRP/ESR, LFTs
- SERUM VIT B12
- NERVE CONDUCTION TEST: measures the speed and strength of the nerve signal
- ELECTROMYOGRAPHY (EMG): where a small needle is inserted through your skin into your muscle and used to measure the electrical activity of your muscles
- EMG AND NCS DONE AT THE SAME TIME

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47
Q

management, prognosis and complications of peripheral neuropathy

A

management and prognosis are dependant on the cause

complications include gangrene, diabetic foot ulcer, heart and blood circulation problems

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48
Q

epilepsy/seizures

A

• A seizure is defined as a transient occurrence of signs and/or symptoms due to abnormal excessive or synchronous neuronal activity in the brain
• Considered to be a disease of the brain defined by any of the following conditions:
1. At least 2 unprovoked (or reflex) seizures occurring more than 24 hours part
2. One unprovoked (or reflex) seizure and a probability of further seizures similar to the general recurrence risk (at least 60%) after 2 unprovoked seizures, occurring over the next 10 years
3. Diagnosis of an epilepsy syndrome

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49
Q

how common is epilepsy/seizures and who does it affect

A
  • 1 in 103 people. 600,000 taking antiepileptic medication
  • Most commonly starts in children or in people older than 60 (bimodal incidence)
  • Epilepsy is much more common in people with a learning disability
  • Epilepsy is often misdiagnosed (20-31% of the time) (usually falsely told they have epilepsy)
50
Q

causes of epilepsy/ seizures

A
  • About two thirds of people in the UK do not have an anatomically identifiable cause = idiopathic epilepsy and is the most common cause of epilepsy in younger people
  • Underlying this is thought to be complex developmental abnormalities in synaptic connections and neurotransmitter distribution and release
  • A genetic predisposition is involved in many people – about 30% of people with it have a first degree relative with it

• Another third have an identifiable anatomical abnormality (this tends to be in the older age group) = symptomatic epilepsy and is caused by cerebral vascular disease, cerebral tumour and post-traumatic epilepsy, less common identifiable causes include perinatal brain injury caused by foetal hypoxia or trauma, cortical or vascular malformation, cerebral abscess or tuberculoma and surgery to the brain

51
Q

risk factors for epilepsy

A
  • Fx
  • Genetic conditions – childhood epilepsy syndromes, or neurocutaneous syndromes such as TB sclerosis or neurofibromatosis
  • Previous febrile seizure (2-7%)
  • Previous intracranial infections
  • Brain trauma esp. penetrating or surgery
  • Comorbid conditions such as CVD or cerebral tumours
52
Q

symptoms/ signs of epilepsy/seizures

A

• SPECIFIC FEATURES OF GENERALISED SEIZURES:

  • TONIC  impairment of consciousness and stiffening (trunk straight or flexed at waist)
  • CLONIC  jerking and impairment of consciousness
  • TYPICAL ABSENCE SEIZURES  which begin in childhood, sharp onset and no residual symptoms, normal activity is interrupted ad the child stares for a few seconds, eyelids may twitch and some very small jerking movements of the hands may occur, lasts 5-10 seconds and usally less than 30, can occur hundreds of times a day in children
  • MYOCLONIC  brief, shock-like contraction of the limbs without the apparent impairment in consciousness
  • ATONIC  sudden brief attacks of loss of tone, associated with falls and LOC

• SPECIFIC FEATURES OF FOCAL SEIZURES:
- FOCAL MOTOR  jerking movement, typically beginning in the face or one hand, and spreading ot involve the limbs, may also present with apparent purposeful movements such as turning the head, eye movements, lip smacking and mouth movements, drooling, or rhythmic muscle contractions, limb weakness may occur for several hours after the seizure
- FOCAL SENSORY  include temporal lobe seizures that may cause sensory, autonomic, emotional, cognitive or other changes
• Secondary generalised seizures start with a focal seizure before spreading to cause a generalised seizure
• Possibly with symptoms of auras (simple partial seizures, no LOC), particularly those arising in the temporal lobe, these include symptoms of unexpected tastes, smells, paraesthesia or rising abdominal sensation

53
Q

DDx for epilepsy/ seizures

A
  • Syncope (e.g. caused by postural changes)
  • Cardiac arrhythmias
  • Panic attacks with hyperventilation
  • Non-epileptic attack disorders
  • In children between 6 months and 5 years: night terrors, breath holding attacks, stereotyped behavioural phenomena and masturbation – especially in those with a learning disability
54
Q

Investigations for epilepsy/seizures

A
  • Lymph node examination
  • If unexplained  consider a very urgent FBC
  • In people >40, with supraclavicular lymphadenopathy or persistent cervical lymphadenopathy, consider an urgent chest X-ray
55
Q

management of epilepsy/seizures

A

• 1st LINE:

  • TONIC CLONIC: if less than 5 minutes  protect pt and do not restrain, if morenthan 5 minutes  buccal midazolam (1st line in community), rectal diazepam (2nd line when buccal midazolam is not available), IV lorazepam if IV access is established and resuscitation facilities available
  • STATUS EPILEPTICUS: buccal midazolam (1st line in community), rectal diazepam (2nd line when buccal midazolam is not available)
  • PREVENTION: drugs given to prevent an attack are specific for the type of seizure  TONIC CLONIC = sodium-valproate, lamotrigine, carbamazepine, topiramate and phenytoin
56
Q

prognosis and complications of epilepsy/seizures

A

prognosis - dependant on cause

complications - death, paralysis

57
Q

bacterial meningitis definition

A
  • Serious inflammation of the meninges caused by various bacteria e.g. strep pneumoniae, Neisseria menigitidis and H. influenzae type b are the predominant causative pathogens in both adults and children
  • Meningitis resulting from infection with Neisseria Meningitides is known as meningococcal disease
  • Meningitis resulting from infection with Streptococcus pneumoniae is known as pneumococcal disease.
  • In neonates (younger than one month of age), Streptococcus agalactia, Escherichia coli, S. pneumoniae, and Listeria monocytogenes are the most common causative organisms
58
Q

how common is bacterial meningitis

A

incidence 2-5 per 100,000

can affect adults and children

59
Q

causes of bacterial meningitis

A
  • Bacteria reach the CNS either by haematogenous spread (the most common route) or by direct extension form a contigious site
  • Neonates can acuire pathogens from non-sterile maternal genital secretions through the placent or from their surroundings
  • Bacteria multiply quickly once they have entered the subarachnoid spae
  • Bacterial components in the cerebrospinal fluid incude the production of various inflammatory mediators, which in turn enhance the influx of leukocytes into the CSF
  • Inflammatory cascade leads to cerebral oedema and increase ICP which contribute to neurological damage and even death
60
Q

risk factors for bacterial meningitis

A
  • Under 5 or over 65
  • Crowding
  • Exposure to pathogens
  • Non-immunised infants
  • Immunodeficiency
  • Cancer
  • Asplenia/hyposplenic state
  • Cranial anatomical defects
  • Cochlear implants
61
Q

symptoms for bacterial meningitis

A
  • Presence of risk factors
  • Headache
  • Neck stiffness – stiff neck with resistance to passive neck flexion (nuchal rigidity)
  • Fever
  • Altered mental status – in older pts this may be the only presenting sign of meningitis
  • Confusion – in older pts this may be the only presenting sign of meningitis
  • Photophobia
  • Vomiting
  • Seizures
  • Infants: hypothermia, irritability, lethargy, poor feeing, apnoea
62
Q

signs for bacterial meningitis

A
  • Kerning’s sign: patient is uspine and the thigh flexed to a 90 right angle, attempts to straighten or extend the leg are met with resistance
  • Brudzinski’s sign: flexion of the neck causes involuntary flexion of knees and hips
  • Non-blanching rash
63
Q

DDx for bacterial meninigitis

A
  • Encephalitis
  • Viral meningitis
  • Drug-induced meningitis
  • TB meningitis
  • Fungal meningitis
64
Q

Investigations for bacterial meningitis

A
  • CSF CELL COUNT AND DIFFERENTIAL: polymorphonuclear pleocytosis
  • CSF PROTEIN: elevated
  • CSF GLUCOSE: low
  • CSF GRAM STAIN: positive
  • CSF CULTURE: positive
  • ANTIGEN DETECTION IN CSF: Neisseria meningitides capsular polysaccharide antigen
  • BLOOD CULTURE: positive
  • FBC AND DIFFERENTIAL: leucocytosis, anaemia, thrombocytopenia
65
Q

management for bacterial meningitis

A

• 1st LINE:

  • ADMIT THE PT TO HOSPITAL AS AN EMERGENCY BY TELEPHONING 999
  • WITH BLANCHING RASH  EMPIRIC Abx: give benzylpenicillin IV, give IM if a vein is not available (inject as proximally as possible preferably into a part of the limb that is still warm as cold areas will be less well perfused)
  • WITHOUT NON-BLANCHING RASH: all people should be transferred directly to secondary care without giving parenteral abx unless urgent transger to hospital is not possible, if this is the case parenteral abx should be administered in primary care  ampicillin
66
Q

prognosis and complications for bacterial meningitis

A

prognosis - with tx, good outcome

complications - shock, elevated ICP, hydrocephalus, seizures, hearing loss

67
Q

Viral meningitis definition

A

• Inflammation of the meninges caused by a vairtey of different viruses and is the most common cause of aseptic meningitis

68
Q

viral meningitis causes

A
  • Enteroviruses are spread by the faecal-oral route
  • Non-polio enteroviruses and arboviruses initially replicate outside the CNS in tissues such as muscle, liver, and the respiratory or GI tacts and then reach the cns by haematogenous spread
  • Viral penetration fo the blood-brain barrier occurs by either infection of endothelial cells or of migrating leukocytes
  • Once within the CNS, viruses spread through the subarachnoid space leading to meningitis and may go on to infect neurons and glial cells leading to encephalitis or myelitis
  • Cellular ummune response to viral infection of the CNS leads to the accumulation of lymphocytes within the CSF and the release of inflammatory cytokines such as IL-6 and tnf
  • The inflammatory response increases the permeability of the blood-brain barrier and this allows diffusion of circulating immunoglobulins into the CSF
69
Q

how common is viral meningitis

A

incidence of 2-5 per 100,000

adults and children

70
Q

risk factors for viral meningitis

A
  • Infants and young children
  • Young adults
  • Older people
  • Summer and autumn
  • Exposure to mosquito or tick vector
  • Unvaccinated for mumps
71
Q

symptoms for viral meningitis

A
  • Presence of risk factors
  • Headache
  • Nausea and vomiting
  • Photophobia
  • Neck stiffness
  • Fever
72
Q

signs for viral meningitis

A
  • Non-blanching rash
  • Kerning’s sign: patient is uspine and the thigh flexed to a 90 right angle, attempts to straighten or extend the leg are met with resistance
  • Brudzinski’s sign: flexion of the neck causes involuntary flexion of knees and hips
73
Q

DDx of viral meningitis

A
  • Encephalitis
  • Meningitis, bacterial
  • Drug-induced meningitis
  • TB meningitis
  • Cryptococcal meningitis
74
Q

investigations for viral meningitis

A

• 1ST LINE:

  • CSF MICROSCOPY: WBC >5 cells/mm^3 for children and adults and >20 cells/mm^3 for neonates
  • CSF GRAM STAIN: negative in viral, positive in bacterial
  • CSF BACTERIAL CULTURE: negative
  • CSF PROTEIN: normal or elevated
  • CSF GLUCOSE: may be low
  • CT/MRI HEAD SCAN: unremarkable, may exclude abscess or bacterial meningitis
75
Q

management of viral meningits

A

• 1st LINE:
- SUPPORTIVE CARE: adequate hydration, use of antipyretics for fever, anti-emetics if vomiting and analgesia for headaches

76
Q

prognosis and complications for viral meningitis

A

prognosis - generally very good

complications - persistent headache and malaise, neuro-developmental deficits in infants

77
Q

migrane definition definition

A
  • Migraine is a chronic, genetically determined, episodic neurological that usually presents in early-to-mid life
  • Pts complain of intermittent headache and associated symptoms such as visual disturbance, nausea, vomiting and sensitivity to light or noise (photophobia and phonophobia)
78
Q

how common is a migraine

A

• Prevalence: 18%, mean age of onset 18years. Men 6% with mean age of onset 14 years.
mainly adults

79
Q

causes of migraine

A
  • Headache of migraine results from neurogenic inflammation of first-division trigeminal sensory neurons that innervate the large vessels and meninges of the brain
  • Causes a change in the way that pain is processed by the brain
  • Increased neuronal activity can be demonstrated in areas of the brainstem during migraine, and this persists even when the headache is relieved by triptans
  • It is not known whether this brainstem activation reflects the cause of migraine (the so called brainstem generator) or instead signifies activation of endogenous pai-control systems
  • When activated, the trigeminal neurons release substances that cause dilation of mnenigeal blood vessels, leakage of plasma proteins into surrounding tissue and platelet actovation
  • This sensitises nerve fibres so that previously ignored stimuli such as the normal pulsations of meningeal vessels are interpreted as painful
80
Q

risk factors for migraine

A
  • Fx of migraine
  • High caffeine intake
  • Exposure to change in barometric pressure
  • Female
  • Obesity
  • Habitual snoring
  • Stressful life events
  • Overuse of headache medications
  • Lack of sleep
81
Q

symptoms /signs of a migraine

A
  • Prolonged headache – a headache that lasts 4-72 hours if untreated is suggestive of migraine
  • Nausea – ‘sick headache’
  • Decreased ability to function
  • Headache worse with activity
  • Sensitivity to light
82
Q

DDx of a migraine

A
  • Tension headache
  • Cluster headache
  • PTSD
  • SAH
  • Cerebral neoplasm
83
Q

investigations for migraine

A

• 1st LINE:
- CLINICAL DIAGNOSIS: diagnosis is based on Hx and physical exam, testing is not used to ‘rule in’ diagnosis of migraine but rather ‘rule out’ plausible alternative diagnoses that are suggested by the pts presentation  FULFILS ICH-IIb CRITERIA FOR MIGRAINE

84
Q

management for migraine

A

• 1st LINE:

  • MILD-TO-MODERATE NSAID/ASPIRIN: aspirin or ibuprofen, pts with nausea + metoclopramide (anti-emetic)  metoclopramide should not be used regularly due to the risk of extrapyramidal side effects
  • SEVERE: triptan e.g. almotriptan, if pt has aura triptans should be taken at the start of the headache and not at the start of the aura
  • If pregnant give paracetamol instead of NSAID/ASPIRIN
85
Q

prognosis and complications of migraine

A

prognosis - do well with treatment

complications - depression, chronic migraine, migrainous infection

86
Q

tension headache definition

A
  • Tension-type headaches can be either episodic or chronic
  • They are rarely disabling or associated disabling or associated with significant autonomic phenonmena, thus patients do not usuallt seek medical care and usually sucessfullt self-treated
  • Pain is typically expressed as being a ‘tight’ band around the head
  • It does not worsen with routine physical activity
87
Q

how common are tension headaches

A
  • Lifetime risk 70-80% (very surprised it’s not higher)
  • About 50% of adults aged 40 years’ experience episodic tension-type headaches
  • The prevalence is higher in woman then men
88
Q

causes of tension headache

A
  • Muscle contraction is often considered the cause of pain in tension-type headaches, but there is little evidence to support this
  • In tension-type headaches, perifranial muscle vontraction is normal or slightly increased and the extent of muscle contraction does not correlate with the extent of head pain
  • Psychological stress is the most common trigger for tension-type headache
  • Extended periods of mental tension or psychological stress may play a role in central desensitisation and the development of chronic tension-type headache
  • Disturbed sleep patterns can trigger an episodic tension-type headache
  • Insomnia and other sleep disorders associated with chronic tension-type headache
89
Q

risk factors for tension headache

A
  • Mental tension
  • Stress
  • Missing meals
  • Fatigue
90
Q

symptoms for tension headache

A
  • Presence of riskf actors
  • Generalised head pain – bilateral pressure like, non-throbbing pain
  • Frontal or occipital head pain
  • Non-pulsatile dull head pain
  • Constricting pain – pain expressed as tight band around head
  • Normal neurological examination – abnormal should prompt investigation for possible causes of secondary headaches
91
Q

signs of tension headache

A
  • No photophobia or phonophobia

* Neck muscle tenderness

92
Q

DDx of tension headache

A
  • Chronic migraine
  • Medicine overuse headache
  • Sphenoid sinusitis
  • Giant cell arteritis
  • Temporomandibular disorder
  • Pituitary tumour/brain tumour
  • Chronic subdural haematoma
93
Q

Investigations of tension headache

A

• 1ST LINE:
- CLINICAL DIAGNOSIS: imaging and lab studies do not aid in the diagnosis of tension-tyoe ehadaches and should only be considered in refractory or progressive cases  typical headache without associated features (nausea, vomitnh), normal neurological exam

94
Q

management of a tension headache

A

• 1st LINE:

  • ACUTE: paracetamol/NSAIDs e.g. ibuprofen/naproxen
  • CHRONIC: antidepressants e.g. amitriptyline
95
Q

prognosis and complications of tension headache

A

prognosis - self tx with simple analgesic medicine is usually effective

complications - peptic ulcer

96
Q

Parkinson’s definition

A
  • Chronic progressive neurological disorder characterised by motor symptoms
  • Parkinsonism is an umbrella term for the clinical syndrome involving bradykinesia together with at least one of the following: rigidity, tremor and postural instability
  • Parkinson’s disease is the most common form of parkinsonism
  • Other causes include: drug induced, CVD, lewy-body dementia, multiple system atrophy, and progressive supranuclear palsy
  • With parkinsons disease, there is a progressive depletion of dpomaine-secreting cells in the substantia nigra but th actual cause is unknown
97
Q

how common is parkinson’s

A
  • Prevalence: 120-230 per 100,000 (0.12-0.23%)
  • 1% of people older than 65 are diagnosed with it
  • 4-8% of people with Parkinson’s are below 50. 1.5X more common in men.
98
Q

causes of Parkinson’s

A
  • Selective loss of nigrostriatal dopaminergic neurons in the substania nigra pars compacta occurs with findings of intracytoplasmic eosinophilic inclusions and neurites both of which are composed of the protein synuclein
  • Loss of striatal dopaminergic output within the circuitry of the basal ganglia accounts for the constellation of motor symptoms
  • Bradykinesia correlates with dopamine feficient with reduced striatal fluorodopa uptake, results in excessive stimulation of the subthalamic nucleus and the GPi which results in slowness and delay initiating movement = symptoms including loss of dexterity, drooling, monotonous voice, loss of facial expression and reduced arm swing
99
Q

risk factors for Parkinson’s

A
  • Increasing age
  • Hx of familial PD in younger-onset disease
  • Mutation in gene encoding glucocerebrosidase (GBA)
  • 1-methyl-4-phenul-1,2,3,6,-tetrahydropyridine (MPTP) exposure – neurotoxin
100
Q

symptoms/ signs of Parkinson’s

A
  • Presence of risk factors
  • Bradykinesia – slowness of movements, progressive reduction in amplitude of repeated movements, delay in initiating movements and freezing of gait are eventually seen in all pts
  • Resting tremor – onset is asymmetrical, chin tremor may occur, tremor may re-emerge when the arms are outstretched
  • Rigidity – hypertonicity is defined as unvarying increased resistance within the range of passive movement about a joint
  • Postural instability – imabalance or falling noted with pull test or spontaneously; retropulsion, common in mild-to-late stage disease
101
Q

DDx for Parkinson’s

A
  • Progressive supranuclear palsy
  • Lewy body dementia
  • Coritcobasal degeneration
  • Alzheimer’s disease with parkinsonism
102
Q

Investigations for Parkinson’s

A

• 1ST LINE:
- DOPAMINERGIC AGENT TRIAL: diagnosis of PD is made clinically and in cases without atypical features no additional diagnostic testing is indicated, if diagnostic testing is warranted due to atypical features or unclear clinical diagnosis, tests may include dopaminergic agent trial  improvement in symptoms

103
Q

management for Parkinson’s

A

• 1ST LINE:
- LEVODOPA: dopa carboxylase inhibitor (co-beneldopa or co-careldopa), usually offered to people in the early stages of parkinson’s disease who motor symtpoms impact on their QOL
• 2ND LINE:
- ORAL MONOAMINE OXIDASE-B INHIBITORS: selegiline, rasagiline, or safinamide
OR
- AMANTADINE

104
Q

prognosis and complications for Parkinson’s

A

prognosis - no cure, about symptom management, course is progressive with rates of progression varying from pt to pt

complications - • Levodopa-induced dyskinesias, motor fluctuations, dementia, constipation

105
Q

multiple sclerosis

A

• Inflammatory demyelinating disease characterised by the presence of episodic neurological dysfunction in at least two areas of the CNS (brain, spinal cord and optic nerves) separated in time and space

106
Q

how common is multiple sclerosis

A

most common cause of neurological disability among young adults
F:M 3:1

107
Q

causes of multiple sclerosis

A

• INFLAMMATION:
- Lymphocytes with encephalitogenic potential are activated in the periphery by factors such as infection or other metabolic stress
- These activated t cells seek entry into the CNS via attachment to a receptor on endothelial cells
- This interaction, mediated by production of matrix metalloproteinases, allows a breach in the blood-brain barrier leading to further upregulation of endothelial adhesion molecules and additional influx of inflammatory cells
- The T cells produce inflamamotry cytokines that cause direct toxicity also attract macrophages that contribute to demyelination
- Epitope spread occurs early and contributes to the complexity of the immunopathology
• DEGENERATION:
- Believed to reflect axonal degeneration and loss
- Demyelination disrupts axonal support and leads to destabilisation of axonal membrane potentials, which causes distal and retrograde degeneration over time
- There is also a suggestion that inflammatory cells, abs, and complement may contribute to axonal injury
- Axonal damage has been identified in regions of active inflammation, indicating that it begins early in the disease process
• Pathologically, MS is characterised by multifocal areas of demyelination, loss of oligodendrocytes, and astrogliosis with loss of axons primarily in the white matter of the CNS, although cortical lesions may also play a significant role

108
Q

risk factors for multiple sclerosis

A
  • Female
  • Northern laititude
  • Genetic factors
  • Smoking
  • Vit d deficiency
109
Q

symptoms/history for multiple sclerosis

A
  • VISUAL DISTURBANCE IN ONE EYE: grayin or blurring of vision in one eye (can be described as looking through pertroleum jelly), may have pain in moving that eye and describe loss of colour discrimination, particularly reds
  • ABNORMAL EYE MOVEMENTS: nystagmus may be present
  • PECULIAR SENSORY PHENOMENA: pts often describe odd sensations of a patch of wetness or burning, or hemibody sensory loss or tingly, in particular banding or hemibanding is associated with spinal cord lesions
  • LHERMITTE’S SIGN: electric shcok-like sensations extending down the cervical spine radiating to the limbs
  • Trigeminal neuropathy or neuralgia
  • FOOT DRAGGING: pts will often describe gradual onset of weakness after walkig several streets or several miles such that the foot slaps the ground – this weakness resolves with rest
  • LEG CRAMPING: involuntary movement in the lower leg with cramping or jerking in the calves, particularly at night or while driving
  • BOWEL DYSFUNCTION: constipation is commonly seen in MS
  • URINARY FREQUENCY: multifactorial causes including damage to the cns resulting in urinary retention and detrusor instability, UTIs are more frequent in pts with urinary retention
110
Q

DDx of multiple sclerosis

A
  • Myelopathy due to cervical spondylosis
  • Fibromyalgia
  • Sleep disorders
  • Vit B12 deficiency
111
Q

investigations for multiple sclerosis

A

• 1st LINE:

  • MRI – BRAIN: hyperintensities in the periventricular white matter, most sensitive images are sagittal FLAIR
  • MRI – SPINAL CORD: demyelinating lesions in the spinal cord, particularly the cervical spinal cord, detection of alternate diagnosis such as cervical spondylosis
  • FBC: should be normal
  • COMPREHENSIVE METABOLIC PANEL: should be normal
  • TSH: normal
  • VIT B12: normal
112
Q

management of multiple sclerosis

A

• 1ST LINE:

- CORTICOSTEROIDS: 3-day high dose of methylprednisolone

113
Q

prognosis and complications of multiple sclerosis

A

prognosis is difficult to say

complications include UTIs, osteoporosis, depression, visual impairment, erectile dysfunction

114
Q

proximal myopathy definition

A

neurological problem which presents as symmetrical weakness of proximal upper and/or lower limbs

115
Q

how common is proximal myopathy

A

relatively uncommon disease

116
Q

causes of proximal myopathy

A
  • PRIMARY: muscular dystrophy (disorders of dystrophin) e.g. Duchenne muscular dystrophy, congenital myopathies (centronuclear myopathy), metabolic myopathies (lipid storage disease)
  • ACQUIRED: secondary metabolic and endocrine myopathies thyroid diseases, parathyroid dysfunction, pituitary dysfunction, corticosteroids, biochemical and DM
117
Q

risk factors for proximal myopathy

A
  • Female
  • Older
  • Hypertension
  • Untreated hypothyrodisim
  • Rnela or hepatic disease
118
Q

symptoms / signs of proximal myopathy

A
  • Weakness predominantly affecting proximal muscle groups (shoulder and limb girdles) is typical
  • Weakness manifests itself in different ways at different ages
  • Reduced muscle strength and power in older children and adults
  • Myalgia may occur in inflammatory myopathies
  • Muscle-strength reflexes are preserved
  • Somatosensory reflexes are preserved
  • Muscle tone normal or reduced
  • Symmetrical proximal muscle weakness
  • Malaise
  • Fatigue
  • Absence of sensory symptoms (paraesthesia)
  • Atrophy of msucles (and reduced reflexes) occurs late with myopathies (early with neuropathy)
119
Q

DDx of proximal myopathy

A
  • Guillain-Barre syndrome
  • Lambert-Eaton myasthenic syndrome
  • Myasthenia gravis
  • Cerebral palsy
  • Spinal muscular atrophy
120
Q

Investigations of proximal myopathy

A

• 1st LINE:

  • FBC
  • URINALYSIS
  • ECG: may show changes of hypokalaemia, increase P-R interval, U waves, wide QRS and non-specific ST-T changes, sinus arrhythmias, deep Q waves and elevated R waves precordially
  • CK
  • U&E’s
  • SERUM MYOGLOBIN
  • ESR
  • ANTINUCLEAR Abs
  • ELECTROMYOGRAPHY: excludes primarily neurogenic processes, proximal muscles of lower extremities often exhibit the most prominent features, often helps to confirm diagnosis but is not in itself diagnostic
121
Q

management of proximal myopathy

A

• 1ST LINE:

  • MYOPATHY ASSOCIATED WITH RESPIRATORY FAILURE: monitor pulmonary function (early restrictive pattern may occur before onset of symptoms), beware of symptoms of nocturnal hypoxia (poor sleep, nightmares, headaches), physio, may require permanent ventilation
  • SPECIFIC MEDICATION MAY BE USEFUL IN PARTICULAR SITUATIONS
  • SURGERY: tendon release surgery to prolong ability to walk
122
Q

prognosis and complications of proximal myopathy

A

prognosis is dependant on the specific diagnosis

complications include respiratory failure, aspiration pneumonia, MSK problems

Core Conditions (13 decks)

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