Neuro

Question 1

TIA definition

Answer 1

Definition

An acute loss of cerebral or ocular function with symptom lasting less than 24 hours caused yb inadequate cerebral or ocular blood supply due to reduced blood flow, ischemia, or embolism.

* Focal, sudden onset neurological dysfunction due to temporary focal cerebral ischemia without infarction 
* A brief episode of neurological dysfunction due to temporary focal cerebral ischemia without infarction

Question 2

TIA epidemiology

Answer 2

Epidemiology

• 15% of first strokes are preceded by TIA
• Male
• Black ethnicity

Question 3

TIA causes

Answer 3

Aetiology

• Athroemobolism from the carotid artery
• Small vessel occlusion
• Cardio embolism result in in micro emboli - left over from an MI, AF, valve disease
• Hyper viscosity - polycythaemia, sickle cell, raised WBC count, myeloma

Question 4

TIA risk factors

Answer 4

Risk Factors

• Age
• Hypertension
• Smoking
• Diabetes
• Heart disease - valvular ischemia, AF
• TIA
• Peripheral arterial disease

Question 5

TIA pathophys

Answer 5

Pathophysiology

• Cerebral ischaemia - lack of O2 and nutrients to the brain
• Ischemia is short lived and lasts 5-15 mins after onset before infarction occurs
• Gradual progression of symptoms suggest a different pathology - demyelination, tumour or migraine

Question 6

TIA symptoms

Answer 6

Symptoms

• Sudden loss of function with complete recovery
• Stroke symptoms - slurred speech, facial drop
• 90% of TIA affect the anterior circulation (carotid artery)- Supplies frontal and medial part of the cerebellum
• weak numb contralateral leg
• Hemiparesis - weakness on entire side of the body
• Hemisensory disturbance
• Dysphasia - inability to speak
• Amaurosis fugax- emboli in the retinal or ophthalmic artery leading to tempory retinal hypoxia and loss of vision in one eye (a curtain descending over the field of vision
• 10% effect the posterior circulation (vertebrobasilar artery - double vision, vertigo, vomiting, chocking and dysphasia, ataxia, hemisensory loss

Question 7

TIA test

Answer 7

1st line test

Diffution weighted MRI or CT is gold standard!
Carotid duplex - look for stenosis
CT angiogram - -look for stenosis
ECG

Question 8

TIA scorning

Answer 8

Scoring systems

ABCD score - max score is 7, a point for each, 4 means high risk
* Age >60
* Blood pressure 140/90
* Clinical features - unilateral weakness, speech disturbance without weakness
* Duration of 60 mins or longer is 2 points, 10-59 mins is 1 point
* Diabetes

If a person has a score of 4, AF, more than one TIA in one week and a TIA whilst on anticoagulation the risk of stroke is very high!!

Question 9

TIA differential

Answer 9

Differential diagnosis

• Impossible to tell from a stoke until there is full recovery
• Hypoglycaemia
• Miranos aura- visual symptoms, sensory symptoms, dysphagia (atypical include motor weakness)
• Subdural haematoma
• Cerebral abscess
• Tumours
• Functional hemiparesis
• Postictial weakness

Question 10

TIA treatmtnet

Answer 10

Management
Initial
Secondary

• Modifiable risks - smoking cessation, less alcohol, exercise, diet
• Refer to specialist for assessment within 7 days of symptoms is low risk and 24 hours if hight risk
• Start statin - simvastatin 40mg
• Antiplatelet - clopidogrel
• Treat raised BP
• No driving until after specialist has seen them
• Aspirin immediately
  *

Question 11

stroke definition

Answer 11

Stroke

Acute neurological deficit lasting more than 24 hours caused by cerebrovascular aetiology

Question 12

stroke epidemiology

Answer 12

• 68-75 is most common age
• Male
  Asian and black African populations

Question 13

stroke causes

Answer 13

• Reduction in cerebral blood flow caused by arterial occlusion or stenosis
• Lacunar - -effects blood flow in small arteries
• Thrombotic
• Embolic
• Cardiac - atherosclerotic disease - smoking, hypertsnsion, high cholesterol, AF, Paradoxical embolisms due to septal defecte
• Vascular - artic dissection, vasculitis, vertebral dissection
  Haem - hypercoagulability- antiphospholipid syndrome sickle, polycythaemia

Question 14

stroke path baed on region affected what symptoms will be presant

Answer 14

• The focal deficit coresponds to the region that is affected
• Anterior cerebral artery stroke effects the feet and legs
• Middle cerebral artery effects hands, arms, face, Broca and wernickes
• Posteroir cerebral artery stroke primarily affects the visual cote which affects a persosn ability to see clearly
  It occurs contralaterally!!

Question 15

stroke symtos

Answer 15

• Anterior cerebral artery - contralateral hemiparesis and sensroy loss with lower limbs and sometimes upper
• middle cerebral artery - homonymous hemianopia, contralateral hemiparesis, aphasia affecting the dominant hemisphere, Hemineglect syndrome: if affecting the ‘non-dominant’ hemisphere; patients fail to be aware of items to one side of space
• Posterior cerebral artery = contralateral homonymous hemianopia with macular sparing
• Vertebrobasilar signs - reduced consciousness, cerebellar signs, quadriplegia/hemianopias

Question 16

stroke catogries

Answer 16

Total anterior circulation stroke (TACS)

All three of the following:
• Unilateral weakness (and/or sensory deficit) of the face, arm and leg
• Homonymous hemianopia
• Higher cerebral dysfunction (dysphasia, visuospatial disorder)

Partial anterior circulation stroke (PACS) Two of the following need to be present for a diagnosis of a PACS:

Unilateral weakness (and/or sensory deficit) of the face, arm and leg
Homonymous hemianopia
Higher cerebral dysfunction (dysphasia, visuospatial disorder)*
*Higher cerebral dysfunction alone is also classified as PACS

Posterior circulation syndrome (POCS) One of the following need to be present for a diagnosis of a POCS:

Cranial nerve palsy and a contralateral motor/sensory deficit
Bilateral motor/sensory deficit
Conjugate eye movement disorder (e.g. horizontal gaze palsy)
Cerebellar dysfunction (e.g. vertigo, nystagmus, ataxia)
Isolated homonymous hemianopia

Lacunar stroke (LACS) One of the following needs to be present for a diagnosis of a LACS:

Pure sensory stroke
Pure motor stroke
Sensory-motor stroke
Ataxic hemiparesis

Question 17

stroke tests

Answer 17

Non contrast CT is first line!!!!
ECG - asses for AF
Bloods - loos for risk factors such as HBA1C, lipids, clotting, and to rule out hypoglycaemia and hyponatremia
Consider ESR, autoantibody in youth
CT angiogram - identify occlusion in patients appropriate for a thrombectomy
MRI of head
Carotid dupler

Question 18

stroke differentials

Answer 18

• Hypoglycemia
• Hyponatremia
• Uremia
• Hypercalcema
• Seizures
• Tumours
  Complictated migrane

Question 19

stroke treatment

Answer 19

• Maintain stable blood glucose levels, hydration sttus and temp
• Antiplatelets - asprin should be give once hemmorage is excluded
• Thrombolysis - alteplase to reestablish blood flow
• Thrombectomy
• Anticoagulatinon should be started, if AF is the causes it should not be started untill 14 days post stroke

Prevention:
* Clopidogrel
* Statin
* Carotis artyer endartectomy/stenting
* Managae hypertension/diabties/smoking

Question 20

stroke prognosis

Answer 20

Totoal anteriro circulation stroke has wort outcomes!

Question 21

Intracerebral haemorrage definition

Answer 21

Definition

Bleeding within the brain parenchyma caused by trauma, hypertension, cerebral amyloid ad arteriovenous malformation. If it does into the brain tissue it is called intraparenchymal and into the ventricles, intraventricular haemorrhage.

Question 22

Intracerebral haemorrage causes

Answer 22

Aetiology

• Hypertention
• Atherlosclarosis
• Vasculitis
• Vascular tumours
• Cerebral amylois angiopathy
• Secondary to ischemaic stroke - blodd vessleis dead causing ti to rupture
• Vasculitis
• Tumours

Question 23

Intracerebral haemorrage risk factors

Answer 23

Risk Factors

• Head injury
• Anyerisms
• Ischeamic stokr
• Anticoagulents such as warfrin

Question 24

Intracerebral haemorrage path

Answer 24

Pathophysiology

• A pool f blood increases pressure in the skull and damages tissues nearby and also from lack of oxygen furher down that route
• It can also lead to herniating

Question 25

Intracerebral haemorrage key presinstations

Answer 25

Key presentations * Headache * Weakness * Seizures * Vomiting * Reduced consciousness * Anterior or middle cerebral - numbness and muscle weakness * Broca - slurred speech * Posterior cerebral artery - vision disturbances

Question 26

Intracerebral haemorrage test

Answer 26

1st line test * CT/MRI * Angiography * Check FBC and clotting

Question 27

Intracerebral haemorrage treatment

Answer 27

Treatment * Intubation, ventilation ICU care if reduced consciousness * Correct clotting abnormalities (give prothrombin if they are on warfarin) * Correct severe hypertension * Relieve intercranial pressure - mannitol * Craniotomy - part of the skull is removed to relive cranial pressure * Stereotactic aspiration - aspirate blood to relive pressure, guided by a CT scanner

Question 28

Subarachnoid hemmorage most common presintation

Answer 28

Patient comes in with a thunderclap headache that really hurts.

Question 29

Subarachnoid hemmorage causes

Answer 29

* Trauma * Atraumatic cases Berry aneurisms (ommunicatinf and anterori arterys at crcle of willis

Question 30

Subarachnoid hemmorage risk factors

Answer 30

* Posy cystic kindye diseases * Coarctatino of the aorta * Ehler-Danlos/marfans * Increasing age * Smoking * Hypertension * Cocaine use Family history

Question 31

Subarachnoid hemmorage pathophysiology

Answer 31

ool of blood increases intercranial pressure leaning to a prevention of blood flow and compression * Blood vessles surronded by blood to start to spasm and constrict * Commoy caused by ruptured berry anyerisms Can causes hydrocephalous as the subarrachnoid space is irritated and leads to scarring and obstructin of cerebrospinal fluid

Question 32

Subarachnoid hemmorage signs and symptoms

Answer 32

* Nerve palsy 3rd and 6th * Reduced GCS * Meningeal irritation Kernig’s sign – unable to extend patient’s leg at the knee when the thigh is flexed Neck stiffness Brudzinski’s sign – when patient’s neck is flexed, patient will flex their hips and knees * Headache - severe, thunderclap * Occipital affecting * Photophobia * Speech changes * Seizures * Weakness * Confusion * Coma * Vomiting * drowsiness

Question 33

Subarachnoid hemmorage tests

Answer 33

* FBC * Serum glucose * Clotting screen * Urgent non contrast CT of the head ECG - look for arrhythmias, ischemia and ST elevation

Question 34

Subarachnoid hemmorage treatment

Answer 34

* Endovascular coiling to prevent berry aneurism rupture * Refer to neurosurgeon * Maintain cerebral perfusion with IV fluids * Nimodipine (CCB) - reduced cerebral artery spasm * Early intervention Monitor for rebleeding, cerebral ischemia, hydrocephalus, hyponatremia

Question 35

Extradural hemmorage most common presintations

Answer 35

There is a head injury, they passed out briefly but seemed fine, a few hours later they start to collapse.

Question 36

Extradural hemmorage pathology

Answer 36

* Head injury - fracture in temporal bone, laceration of middle menignela artery Blood accumulates rapidly over mins t hours between bone and dura

Question 37

Extradural hemmorage key presintations

Answer 37

* Head injury * Loss of consiocusness following the trauma * Lucis interval and then a decreases in pressure * Bradycardia and raised BP * Decreasing GCS * Coning of being throgh foramen magnum * Death due to resp arrest Brain displacement - raised ICP, herniatino -supreatentonial (cerebellum pushed against skull or tentorium

Question 38

Extradural hemmorage tests

Answer 38

* CT scan - shows biconcave haematoma adjacent to skull Skull x-ray = may sow precure lines

Question 39

Extradural hemmorage differential

Answer 39

* Meningitis * Carotid dissection * Epilepsy * CO poisoning Subdural haemorrhage

Question 40

Extradural hemmorage treatment

Answer 40

* Refer to neurosurgeon * Burr hole craniotomy * Legation of bleeding vessel * Stabilise patient - ABCDE IV mannitol

Question 41

subdural hemmorage common presintation

Answer 41

An elderly alcoholic comes in 2 weeks after falling down the stairs.

Question 42

subdural hemmorage definition

Answer 42

Rupture of the brigding veins between eth superioir surface of the brain and the saggital sinus

Question 43

subdural hemmorage epidemiology

Answer 43

* Small brain - alcoholics or dementia * Shaken babies Elederly patients

Question 44

subdural hemmorage causes

Answer 44

* Contusions/lacerations * Base of skull fracture * Vertebral artery rupture/dissection Intravascular haemorrhage

Question 45

subdural hemmorage risk factors

Answer 45

* Traumatic head injury * Age * Alcoholics Shaken baby syndrome

Question 46

subdural hemmorage path

Answer 46

* Trauma due to deceleration in violent inhury ot dural metasrases or bleeding of the bridging veins between cortex and venous sinus * Bridgin viens bleed and form a haemaoma between dura and arachnoid this reducedes pressure and the bleeding stops. * Days/weeks later the haematoma starts to autolyse and there is a massive increases in oncotic and osmotic pressure and there is a gradual reise in cranial pressure This shifts strutres away from eth midlien and can causes herniatino if left untreated

Question 47

subdural hemmorage signs and symptoms

Answer 47

* Personality change * Raised ICP * Herniatin * Vomiting * Headache * Fluctutaing levels of consciousness * Vomiting * Focal neurology, hemiparesis and sensory loss

Question 48

subdural hemmorage

Question 49

subdural heamorrage differential

Answer 49

* Stroke * Dementia * CNS mass Subarachnoid haemorrhage

Question 50

subdrual heamorrage treatment

Answer 50

* Refer to neurosurgeon * Burr hole craniotomy and irrigation/removal of haematoma * Stabilise patient * IV mannitol to reduce ICP

Question 51

what is teh eye thing with strokes

Answer 51

* Amaurosis means dark in greek and fugax meannf fleeting in latin * Most commonly cuased by an atherosclerotic emboli that block the blood flow * It is temporary loss of vision which returs soon * It comes down like a shutter but then returs slowly after several mins Statin and asprin/clopidogrel

Question 52

Meningitis definition

Answer 52

Inflammation of the arachnoid and pia mater due to a viral (80%), bacterial or fungal infection.

Question 53

Meningitis causes

Answer 53

* N.Meningitidis and S.pneumonaiae are the most common bacterial * Enterovirus and Coxsackie are the most common viral * Neonatal - Group B strep, E.Coli, listeria Monocytogenes * Children - N.meningitidis, S.pnumonia, H.influenza * Adults - S.pumonia, N.meningitidus * Elederly - s.pnumonia, N. menigitidis, listeria monocytogenis * Immunocompramised - listeria monocytogenes, M.tuberculosis * Enterocirus: coxsackie and achovirus * Herpes simplex - 2 * Varicella Zoster virus Fungal- * Crypotococcus neoformans Candida

Question 54

Meningitis risk factors

Answer 54

* Immunocompramised (children and elderly, HIV, chemotherapy) * Non immunised - risk fo H.influenza, pnumococcla and meningiococcal Crowded enviroment - students in halls of residance

Question 55

Meningitis path

Answer 55

Pathophysiology * Direct spread: pathogen gets into the skull or spinal Colum and penetrates the meninges, normally a defect such as spinal bifida, or skull fracture * Haematogenous spread - pathogen enters the bloodstream and crosses through the BBB into the CSF * Once the pathogen is in th CSF it starts multiplying and the WBC also start multiplying and so is a microleitres of CSF contains more than 5000 WBC then it is meningitis * The additional immune cells attrcat more fluid and start casuing local destruction as they try to controll the infection * This causes the pressure to rise, glucose to fall and protien lecels to increase * Bacteria and viruses causes acute menigngitis and fungi causes chronic * Symptoms occur within 3-7 days of exposure ot the pathogen

Question 56

Meningitis signs

Answer 56

Signs * Kernigs sign - when hips is felexed at 90, extension of the knee causes pain * Brudzinski sign - severe neck stiffness causes the hips and kness to flex when the neck is flexed * Petechial or pupuric non blanching rash * Pyrexia * Reduced GCS

Question 57

Meningitis symotoms

Answer 57

Symptoms * Headache * Photophobia * Neck stiffness * Fever * N&V * Seizures

Question 58

Meningitis test

Answer 58

1st line test * FBC - leukocytes * CRP - raised * Blood glucose to compare wih CSF glucose levels * Blood culture * Blood pcr for N. meningitidis * CSF gram stain - s.pnumoniae, N.meningitidis * CSF culture * CSF PCR - HSV, and VZV * CSF - low glucoxe, high protiens, high WBC cont

Question 59

Meningitis tx

Answer 59

Treatment * Primary care: IV benzylpenicillin STAT one off dose and transmission to hospital Bacterial: * Dexamethasone - reduced likelihood of neurotically sequelae * Empirical - IV cefotaxime (and amoxicillin if under 3 months or over 50 years) * Meningococcal - IV benzylpenicillin (or ceftotaxime) * Pneumococcal or Influenzas - IV cefotaxime * Listeria monocytogenes - IV amoxicillin and gentamicin Viral: * Aciclovir - HSV, VZV * Conservative management Contact tracing: * Meningitis and meningococcal are notifiable diseases in England! * Consider antibiotic prophylaxis for people with prolonged close contact for 7 days previously * Ciprofloxacin and rifampicin * Meningococcal vaccine

Question 60

Meningitis complications

Answer 60

Complications * Abscess * Cerebral oedema * Seizures * Memory loss * Cerebral palsy * Long term conative and behavioural deficit

Question 61

Encephalitis definition

Answer 61

nflamation of the brain parenchyma, mostly frontal and temporal lobes.

Question 62

Encephalitis causes

Answer 62

* Herpes simplex virus 1 and 32 (most common- 95%) * Varicalle zoster * Epstien barr * Cytomegaolivrus * HIV * Syphyliss * Tuberculois s

Question 63

Encephalitis risk factors

Answer 63

* HIV * Mosquito bite * Immunocompramsied Close contact with cats - toxoplasmosis

Question 64

Encephalitis path

Answer 64

* Immune response to the invasion of a pathogen causing inflamation I the brain tissue HSV gets into the sensoey ganglia and travles into the skin, howvere it can work bac to the CNS and causes encephalitis, this is notmallt down the olfactory or trigeminal nerves

Question 65

Encephalitis signs and symptoms

Answer 65

* Pyrexia * Reduced GCS * Aphasia * Hemiareses * Cer - **May also have signs of meningitis:** - meningo-encephalitis * Fever * Headache * Fatigue * Confuction * Seizures * Memory disturance * Withdrawal or change in personality

Question 66

Encephalitis test

Answer 66

* FBC, CRP, U&E, blood culture * HIV serology * Throat swab for virusses * MRI of head to show inflamation of medial temporal and inferior frontal lobes * CSF investigations - lymphocytosis and raised protiens, PCR for viruses, culture for bacteria, serology got anibodies

Question 67

Encephalitis treatment

Answer 67

* Aciclovir to all * Gancicovit - HHV6 infection * A combination of ganciclovir and foscarnet is usually used in CMV

Question 68

Encephalitis complications

Answer 68

* Seizures stroke * Changes to memeory * Chronic pain * Learning disabilitys * Hormonla imbalance * Hydocephalous * Storke

Question 69

MS definition

Answer 69

Definition Chronic autoimmune T cell medicated inflammatory disorder of the CNS in which there are multiple plaques of demyelination within the brain and spinal cord occurring sporadically over years.

Question 70

MS epideimiology

Answer 70

Epidemiology * Women 2x as likely to get it * More common further from the equator - possible vit D link * 20-40 age of onset

Question 71

MS RF

Answer 71

Risk Factors * MS prevalence rate can be altered by a change in enviroment so is not purle genetic * Age f migration is critical for risk retention * Genetics - HLA - DR2 * Exposure to EBV! * Females more

Question 72

MS pathophysiology

Answer 72

Pathophysiology * Type 4 hypersensitivity reaction (cell mediated) of the CNS * Myelin produced by oligodendrocytes is attacked by T cells and active B cells to produce autoantibodies against myelin * Once t cells can cross the BB barrieer they causrs a cascade and destruction to the neuronla cells of the brain * This results in demylenation and condution dysfunction * Mylein sheath begins to regenerate but it is less deficient * When exposed to hight heat conduction through the new myelin drastically decreases * for example there is a loss of myelin around the optic nerve, this causes sight loss, but the myelin slowly grows back, this causes sight to return partially but in hot showers it might go blurry again as the hear disrupts the new myelin * Uhthoff’s phenomenon – worsening of neurological symptoms in MS when body gets overheated from hot weather, exercise, saunas and hot tubs * Plaques of demyelination are periventricular (around a vein) and occur everywhere in the CNS but commonly around the optic nerve, ventircels, corpus callosum, brainstem and cerebellum, cerviival spinal cord * There are active and inactive Active * Demylenation - breakdown priducts resant * Variable oligodendrocytes * Hypercellular plaue edge * Perivenous inflamatory infiltrare - macrophages and T lymphocytes * Extensive BBB disruptio * Older plaques may have centreal gliosis Inactive * Demylenation - breakdown pruductes absent * Variabe oligodendrocyte loss * Hypocellular plaque * Variable inflamatory infiltrate * Pluaqes gliosed * Moderate to mine BBB disruption

Question 73

MS key presintations

Answer 73

Key presentations * Pattern 1 - macrophage mediated * 2 - antibody mediated - lots of inflamation and plasma exchange is needed * 33 distal oligodenrogiopathy and apoptosis - toxic, virus induced * 4 - primary oligodendrioglia degeneration (metabbolic causes)

Question 74

MS types

Answer 74

* Relapsing remitting - most common - clearly ddefined releapse and full/partial recovery,perioids of no increase I disease * Primary progressive - diseases prognression from onset constantly * Secnorary progressive - initial repape sremitting byt tehn continuous preogression Progressive relapsnig - progressive from onset- with acute relapseswith perioids in relapses characterised by continous preogression

Question 75

MS signs ans symptoms - there is a mnumonic

Answer 75

Signs LOSS NB * Lhermitte’s sign (electric shock sensation on fefxtion of the neck) Optic neuritis – impaired vision and eye pain Spasticity and other pyramidal signs Sensory symptoms and signs Nystagmus, double vision and vertigo Bladder and sexual dysfunction * Exasrbated by hear - uhthoffs phenomenon Symptoms * Dependson the region affected * Charcots triad -dysarthia (plaques in the brainstem), diffullt or unclear speech * Intention tremor - ataxia, tremors, mucles weakness and sapsms, paralysis * Nystagmus - plaques in the nereves of the eyes, double visison * Cerebral hemisphere- silent lesions, depends on eth hemisphere * Spinal cord ○ Lhermitte’s sign – electric shock runs down back and radiates to limbs ○ Bladder and sexual dysfunction ○ Weakness ○ Paraplegia ○ Spasticity ○ Tingling ○ Numbness * Optic nerves ○ Impaired vision ○ Eye pain * Medulla and pons ○ Dysarthria ○ Double vision ○ Vertigo ○ Nystagmus * Cerebellar white matter ○ Dysarthria ○ Nystagmus ○ Intention tremor ○ Ataxia

Question 76

MS tests

Answer 76

1st line test * 2 or more CNS lesions disseminated in time and space - this means need to be two separate parts from brain, spinla cord, optic nerve and it needs to be spaced out over a year Gold standard test * MRI with contrast - acitve lesios will take up contrast and appear white in colour r * Lumbar puncture CSF electrophoresis - inflammation is confined to NS, inflammatory proteins found in the CNS * Evoked potentials - to test how long it takes impulses to travel. There should be delayed visual, brianstem, auditory and somatosensory potentials

Question 77

MS differential

Answer 77

Differential diagnosis * Lupus * Sjorgrens * Polyarteritis nodosa * Lyme disease * Syphyliss * Aids * Cardiac embolic event

Question 78

MS treatment

Answer 78

Treatment * No cure * For acute relapsing remitting - IV methylprednisolone For chronic * SC beta interferon (can causes injection sight reactions, flu syptoms, mild lymphopenia, raised liver enzymes) * Glatiramer acetate * Diseases modifying drugs: * IV alemtuzumab - CD52 monocolnal antibody that acts on T cells * IV natalozumab - stops t cells form being abel to cross the BBB Symptom manegemtn: * Tremor - Beta blocker * Muscle spacitiy - diazapam, alcohol, botilium toxin * Sever - intrathecal baclofen or functional neuorguery * Removal of triggers - UTI, bed sores * Physio * Wrist bands with weight * Neuropathic pain - gabapentin or amitriptyline

Question 79

GBS definition

Answer 79

Definition Acute inflammatory demyelinating (or attacking the axon) polyneuropathy affecting the ONS (Schwann cells) following an upper Resp/GI infection

Question 80

gbs epidemiology

Answer 80

Epidemiology * Males * 15-35 and 50-75

Question 81

gbs causes

Answer 81

Aetiology * Campylobacter jejuni * EBV * Cytomegalovirus * HIV * Zoster

Question 82

gbs path

Answer 82

Pathophysiology * Campylobacter jejuni, EBV or CMV have the same antigesn as schwann cells and aues autoantibody mediated damage to the myelin sheath du to molecular mimicry * Nerve cell damage consists of segmental demyelination causing a reduction in peripheral nerve conduction and acute polyneuropathy * There is: demylenatinf, axonla sensorimotor, and axonal

Question 83

gbs risk factors

Answer 83

Risk Factors * Resp or GI infection 3 weeks before onset * Vaccinatios * Post pregnancy

Question 84

gbs signs and symptoms

Answer 84

Signs * Sweating * Raised pulse * Postral hypotension * Arrhythmias * Symetrical ascending muscle weakness * Proxinmal muscles are more affected * Relexes lost early in illness Symptoms * Paraesthesia and numbness * Msucle wekaness * Back and limb pain * CN involvement - diplopia and dystharia * Resp - affects diaphragm *

Question 85

gbs test

Answer 85

1st line test * Lumbar puncture at L4 - CSF raised protine bt normal white blood cell cout * Nerve conduction studies - shows slow conduction, prolonged distla motor latency and conduction block * Lung funciton tests - monitor FVC to see if there is resp involvement

Question 86

gbs differential

Answer 86

Differential diagnosis * Hypokalaemia * Myasthenia gravis * Botulism

Question 87

gbs treatment

Answer 87

Treatment * IV immunoglobulins * Plasma exchange * Supportive care * VTE prophylaxis- pulmonary embolism is leading cause of death)

Question 88

gbs prognosis

Answer 88

Prognosis 80% will fully recover 15% will have sligt nerve damaeges permenantly 5% mortality

Question 89

Parkinsons definition

Answer 89

Definition Loss of dopaminergic neurons within the substania nigra-pars compacta and the basal ganglia Definition Loss of dopaminergic neurons within the substania nigra-pars compacta and the basal ganglia

Question 90

Parkinsons epidemiology

Answer 90

Epidemiology Second most common neurodegenerative after Alzheimer's Male

Question 91

Parkinsons risk factors

Answer 91

Risk Factors Age Gender - men are 1.5 time smroe likely to develop Family history Oxidative stress Mitochondrial

Question 92

Parkinsons path

Answer 92

Pathophysiology * Progressive reduction in DA in BG leading to movement disorders * Genes which code for alpha-synlucin are wrong causing misfolding the accumulatin of lewy bodies * Bradykinesia, tremor, rigidity, postural instability * Assciated with lwy body dementia, multiple system atrophy and progressive supranuclear palsy * Less da means that the thalamus is inhibited and there will be intracytoplasmic inclusino bodeis * Tyrosine 🡪 L-dopa 🡪 dopamine 🡪 dopamine receptor

Question 93

Parkinsons key presintations

Answer 93

Key presentations Normally it start with motor symptoms which are unilateral, that then become bilateral, and then mental symptoms set in as well. * Bradykinesia * Tremor * Rigidity * Slow movement (bradykinesia) * Difficulty initiating movement * Shuffling gait ad resuced arm swing * Resting tremor 'pill rolling' * More prounonced on resting and imporved on movement * Rigidity - cogwheel rigidity due to tremor, lead pipe rigidty is stiffness throughout entrie movement * * Micrographia - abnormal, small, cramped handwrighting * Hypomimia- reduced facial expressions * Postural instability * Ansomia - smell blindness * Sleep disturbace * Depression * Anxiety * Dementia * Constipation

Question 94

Parkinsons test

Answer 94

1st line test * Clinical diagnosis - bradykinesia and at least one of: tremor, rigidity, postural instability. * MRI of brain to exlude other diagnosis - show substantia nigra atrophy * SPECT (DaT scan): single-photon emission computed tomography (SPECT) will show reduced dopamine uptake in the basal ganglia

Question 95

Parkinsons differential

Answer 95

Differential diagnosis Benign essential tremor * Incontinence, dementia, symmetry, early falls, tremor in action are signs that it is NOT Parkinson's * Might be normal pressure hydrocephalouhs * /

Question 96

Parkinsons treatment

Answer 96

Treatment * Levodopa (DA precursor) and decarboxylase inhibitor - * /Monoamine oxidase B inhibitor(inhibit enzymatic breakdown of DA) - sleglinine, raseaglinein - stops breakdown of circulating dopamine

Question 97

Parkinsons complications

Answer 97

Other notes There are different speeds of release from the L-Dopa drug - quic reease, slow release over the curse of the day.

Question 98

Huntington's definition

Answer 98

Definition A neurodegenerative disorder caused by a lack of GABA. Chorea - continuous flow of involuntary jerky, semipurposful movements flitting form one part of the body to another. They may interfere with voluntar movements durinf sleep

Question 99

Huntington's epidemiology

Answer 99

Epidemiology * Autosomal dominant condition with full penetracne - all gene carries will develop the gene * Presets in middle age initially with a prrodroma phase of mild symptoms - irratibility, depression, incoordination and tehn pregress to psychiatric ad connitive symptoms

Question 100

Huntington's causes

Answer 100

Aetiology Mutation of chormosome 4 leading to repeated expression of CAG There needs to be >36 triplets to be diagnotsic of hunntington.

Question 101

Huntington's path

Answer 101

Pathophysiology * Repeated CAG sequence leadingto expanded polyglutamine repeate * The more CAG repeates there are, the earlier the symptoms present * 36-55 * Anticipation- -repeats more in each generation * There is a faulty hunntington builduo in e striatum leading to cell death and loss of cholinergic and GABA nueric neurons theis leads to decreased ACH and GABA synthesis in the striatum * Less GABA regulation of dopamine ot the stratum causing excessive thalamic stimulation increased movement.

Question 102

Huntington's key preintatino s

Answer 102

Key presentations 1st phase - * Depression * Incoordination * Personality changes 2nd stage - * Chorea - dance movements * Abnormal eye movements * Loss of coordination * Dysphasia * Dysarthria * Dementia * Depression * Rigidity

Question 103

Huntington's test

Answer 103

1st line test * Genetic testing - shows CAG repeats * MRI/CT- shows atrophy of striatum - caudate and putamen and nicreased size of frontla horns of laterla ventricles

Question 104

Huntington's differential

Answer 104

Differential diagnosis * Sydenhams choea - rheumatic fever * SLE * Basal ganglia stroke * Wilsons disease

Question 105

Huntington's treatment

Answer 105

Treatment * Antipsychotics - risperidone for chorea and agressiev behaviour * Benzodiaipenes * Sulpridie - depress never function * Depression - SSRIs * Tetrabenzine can be used to deplete dompam Most common death is from aspiration pneumonia or suicide

Question 106

alzheimers eipdeimology

Answer 106

Epidemiology * 50-75% of dementias * Females

Question 107

alzheimers risk factors

Answer 107

Risk Factors * Age * Genetics * Cardiovascualr disease * Depression * Low education * Low socia suppirt * Head traumas

Question 108

alzheimers path

Answer 108

Pathophysiology * Inturruptinos of key neuronal preocese leading to cell deat * Senile plaques: depositis of beta amyloid extracellularly * Neurofibrillary tangle - aggregation of hyperphphrylated Tau protiens - neurofibrillary tangles intracellularly causing apoptosis

Question 109

alzheimers key presintations

Answer 109

Key presentations * Poor memory * Language problems * Executive functioning problems * Disorientation * emotional lability (exaggerated changes in mood) * Depression * Anxiety * Apathy * Sleep cycle disturbace * Motor disturbance * Psychosis * Loss of independacne

Question 110

alzheimers test

Answer 110

1st line test * Mini mental state examination MMSE - to asses attention, con, languae, execuative function, visospatial function, recent and remote memory * Montreal cognitive assessment scale (MoCA) * ECG * Virology * Chest X ray * CT/MRI DSM-V * Inability to carry out nornal functinos * Imparement in >2 cognitive domains * Differential excluded- delerium, psychiatric disorders * Severity is socred using the montreol congbintive assesment tool and minin metla stae examination *

Question 111

alzheimers differential

Answer 111

Differential diagnosis Other dementia Depression Delerium

Question 112

alzheimers tx

Answer 112

Treatment * Exercise * Aromatherapy * Use of music/dancing * Programs to maintain cognitive function * Mild - moderate- acetylcholiesterase inhibitor - donepezil/rivastigmine * Moderate - severe - N-Methtl-D-aspartic acid receptr antagonist (memantine) * End of life care

Question 113

Frontotemporal dementia definition

Answer 113

Neurodegenerative disorder characterised by focal degeneration of the frontal and temporal lobes. Heterogenous condition with various subtypes.

Question 114

Frontotemporal dementia epidemiology

Answer 114

* Makes up 2% of dementias * Affects patent at a younger age - 65 Mena onset is 58

Question 115

Frontotemporal causes

Answer 115

Frontl and temporal atrophy with loss of ver 70% of spindle neuros

Question 116

Frontotemporal dementia risk factors

Answer 116

* Family history - strong genetic predisposition - microtubule associated protine Tau -MAPT is on chromosome 17 and leads to prpensity of Tu and formation fo neurotocix aggregates * Granulin precursor C9ORF72 - on chromosome 9 and is the most common causes og inherited FTD

Question 117

Frontotemporal dementia path

Answer 117

* Tau protin gets hyperphosphorylates which chages tehris shapesand stops them from being able to tie together the tubulins the the neuron cytoskeleton * They start clumping togetehr and forming pick bodies * Neurns get damaged and undergo apoptosis More and more neurons die causing atrophy and widening ventricles

Question 118

Frontotemporal dementia key presintations

Answer 118

Frontal lobe effects: * Disinhibition - socially inappropriate behaviour * Loss of empathy * Apathy * Hyperorality - eating beond satiety, consuming non edible things * Compulsive behaviour - cleaning, checking, hoarding Temporal lobe effects: * Effort in speech * Apraxia - diffeculty in articulation * Word finding difficulty * Surfae dyslexia/dysphragia - misprounoncing words Atrophy progressino cauing: * Memory loss * Lack of conc * Inibility to learn new things

Question 119

Frontotemporal dementia test

Answer 119

* Cognitive assessment * MRI - shows changes in temporal and frontal lobes Brain biopsy after death

Question 120

Frontotemporal dementia tx

Answer 120

* Non pharmaceutical - exercise, physiotherapy, speech and language therapy, behaviour modification Pharmaceutical - SSRI, atypical antipsychotics

Question 121

lewy body dementia definition

Answer 121

Neurodegenerative disease characterised by fluctuating cognitive impairment, visual hallucination and parkinsonism.

Question 122

lewy body dementia risk factros

Answer 122

* Older age * Male Family history

Question 123

lewy body dementia pathophys

Answer 123

* Neurons contain a protien called alpha synuclein and this get smisfolded. This isfolded alpha-synuclein aggragtes to from lewy bodies that deposit inside neuronsin te hcortex and substantia nigra This causes neurons to die

Question 124

lewy body dementia key presintations

Answer 124

Early symtoms: * Difficulty focusing * Poor memory * Visula hallucinations * Disorganised speech * Depression Later symptoms (mimick Parkinson) * Resting tremor * Still and slow movements * Reduced facial expression Sleep disorders

Question 125

lewy body dementia test

Answer 125

* Diagosis is based on pattern of symptoms * FBC, U&E, ESR, B12, folate, TSH, glucose and thiamine to exclude other causes Diagnosis provided in brain autopsy showing lewy bodies

Question 126

lewy body dementia tx

Answer 126

* Domapine analouge - levodopa Cholinesterase inhibitors - donepezil incfreases ach availability

Question 127

vascular dementia definition

Answer 127

Chronic pregressive diseases, it is common form of dementia cuases y cerebrovascualr disease.

Question 128

vascular dementia epidemioloy

Answer 128

* 20% of dementias * Often mixed with altzeimers

Question 129

vascular dementia causes

Answer 129

* Vascular brain injury or dysfunction as a result of conditions that impari cerebral blood flow * Ischeamic stroke * Small vessel disease * Haemorrhage Cerebral amyloid small vesse disease

Question 130

vascular dementia path

Answer 130

* Vascualr dementia is prigressive loss of breain function cuases by poor blood flow, tyrpicaly a series of strokes * Leads to gradual ischemia. Small plaques can break off and block vessles and blood flow, alnd arteris can athersclarose shut too This causes necoris sand dementia

Question 131

vascular dementia key presintaions

Answer 131

* Symotoms of dementia that appear suddenly and are stepwise in decline (after each stroke) * Poor langueag e * Poor memory * Probems with panning and problem sloving * Dioriontation * Agitation * Sleep disturbace * Spression/anxiety * Apathy * Psycholsis * Motor disturbance

Question 131

vascular dementia test

Answer 131

* Neuropsycholoicgal test to asses function * Blood tests and examinations - ECG, virology, chets xrya CT/MRI to exclude other pathologies

Question 132

vascular dementia tx

Answer 132

* No cure or medication * Manegement of RF - smoking, hgh BP< diabeties, cholesterol * Acetylcholinesterase inhibitors - in mixed dementia End of life care

Question 133

migrane definition

Answer 133

Definition * Recurrent throbbing headache often preceded by aura, associated with vomiting, nausea and visual changes * It might causes visual phenomena such as zig zag lines, shimmering or scotomas, and pins and needles. Weakness of the limbs and motor function.

Question 134

migrane epidemiology

Answer 134

Epidemiology * Most common causes of episodic headache * Females

Question 135

migrane causes

Answer 135

Aetiology CHOCOLATE * Chocolate * Hangovers * Orgasms * Cheese * Oral contraceptives * Lie-ins * Alcohol * Tummult - fluid noise * Exercise Mensturation, red wine and bright lights as well

Question 136

migrane risk factors

Answer 136

Risk Factors * Family history * Female * Age

Question 137

migrane path

Answer 137

Pathophysiology * Change in brainstem bloodflow leads to instable trigeminal nerve nucli in the basal thalamus leading to release of vasoactive neuropeptides, CGRP and substance P * Leads to neurogenic inflammation, vasodilation and plasma protein extraversion * Headache is due to euronal hyperexcitiability causing a dilation of meningea blood vessles and senstisation fo nereve fibres * Aura is caused yb corticla spreading depression cuasing hypersensiivoty to certain stimuli

Question 138

migrane duagnosing types

Answer 138

Diagnosing Migraine without aura * 5 attacks fulfilling below criteria * Attacks last 4-72 hours * Unilateral, pulsating, moderate, aggravated by routine physical activity * Nausea/vomiting/photophobia and phonophobia Migraine with aura - * At least 2 attacks * Reversable aura symptoms - zigzags, spots, aphasia, tingling and numbness, motor weakness * Aura spreads gradually over 5 mins the aura lasts 5-60 mins, more than one is unilateral

Question 139

migrane test

Answer 139

1st line test * Mainly clinical * Examine eyes for issues, BP, head and neck * Exclude other causes - lab test for ESR ad CRP * REDFLAGS - thunderclap headaches, change in pattern of migraines, abnormal neuro exam, onset after 50 years, epilepsy, posteriorly located headache * Lumbar puncture indications

Question 140

migrane differential

Answer 140

Differential diagnosis * Tension headache * Cluster headache * Medication overuse headache * Subarachnoid haemorrhage * Tumour

Question 141

migrane tx

Answer 141

Treatment * Avoid triggers * Acute attacks - mild NSAIDS/paracetamol/antiemetics * Prophylaxis - propranolol to topiramate (anticonvulsant) * Acupunctures * Amitriptylin (antidepressant) * Botulinum toxin type A -

Question 142

tension headache definition

Answer 142

Chronic daily, recurrent headaches. More of a dull ache

Question 143

tension headache epidemiology

Answer 143

* Common primary headache * (<15 days/month) or chronic (>15 days a month for at least 3 month) Onset tends to be in the 20s

Question 144

tennsio headaceh causes

Answer 144

Neurovascular irritation which refers to scalp muscles and soft tissue MD SCOLD * Missed meals * Conflict * Stress * Clenched jaw * Overexertion * Lack of sleep Depression

Question 145

tension headache rf

Answer 145

Stress Sleep deprivation Bad posture Hunger Eyestrain Anxiety Noise

Question 146

tension headache path

Answer 146

* May be sue to muscle ache in the frontaisl , temporalis and occipital muscels * Increased tenderness f the pericarnial myofascial structure leads to nociceptors leading to episodic tension heasaches

Question 147

tension headache diagnosis types

Answer 147

* Infrequent is > 10 attacks occurring <1 day/month (<12 days/year) and fulfilling B-D * Frequent is >10 episodes of headache occurring 1-14 days/month for an average of 3 months * Chronic - more than 15 days in a month for 3 months * B - Headache lasting from 30 minutes to 7 days * C – headache has two of the following Bilateral Pressing/tightening (non-pulsatile) quality Mild or moderate intensity/pain Not aggravated by routine physical activity (e.g. walking or climbing stairs) * D – both of the following No nausea or vomiting (anorexia may occur) No more than one of photophobia and phonophobia E – not attributed to another disorder

Question 148

tension headache key presintations

Answer 148

* Bilateral pressing/tight sensation * Nausea and vomiting Phonophobia and photophobia

Question 149

tension headache test

Answer 149

* Patients is asked to keep a headache diary * CT or MRI of the head ESR to rule out giant cell arteriti

Question 150

tension headache differential

Answer 150

* Migraine * Cluster headache * Giant cell arteritis Drug induced headache - wort when on analgesia such as opioids

Question 151

tension headache tx

Answer 151

* Reassurance lifestyle advice * Stress relief * Avoidance of cause * Paracetamol and NSAIDS but for no more than 6 days a month t reduce medication overuse headaches * Tricyclic antidepressants - amitriptyline * Hot towels on area Acupuncture and massage

Question 152

cluster headache definition

Answer 152

Most disabling of the primary headache disorders - intensely painful!!

Question 153

cluster headache epidemiology

Answer 153

* Much rarer than mirage * Males more * 20-40 years * Smokers

Question 154

cluster headache causes

Answer 154

* Autosomal dominant gene is involved

Question 155

cluster headache risk factors

Answer 155

Male Smokers Alcohol

Question 156

cluster headache path

Answer 156

* Trigeminal autonomoc cepalica are are though to occur due to hypersensitivity arc resulting in vascualr dilation nd trigemincal nerve stimulation Can be episodic followed by pain free perioids or chornic with no substantial remission

Question 157

cluster headache diagnosis tyes

Answer 157

* Episodic - > 2 cluster periods lasting 7 days to 1 year separated by pain free periods lasting > 1 month Chronic – attack occur for > 1 year without remission or with remission lasting <1 month

Question 158

cluster headache ke presintations

Answer 158

usters headaches * Unilateral periorbital or temporal headaches * Ipsilateral autonomic symptoms * Lacrimation, nasal congestion and discharge, ptosis (eyelid drooping), miosis (constriction of the eye) * Nausea and vomiting * Photophobia Agitation and restlessness

Question 159

cluster headache test

Answer 159

* MRI /ct to rule out underlying cuases ESR - rle ot giant cell arteritis

Question 160

cluster headache differental

Answer 160

* Migranes * Trigeminal automonim ceohalagias * Trauma * Idiopathic intercranial hypertension * Subarachnoid haemmore * Space occupying lesisons * Giant cell arteritis * Venous sinus thrombosis Malignant hypertension

Question 161

cluster headache tx

Answer 161

* Referred to a neurologist * Triptans - 5HT 1B/D agonists - provide symptomatic relief within 15 mins for 75% of patients * High flow oxygen - provides relief * Avoinf - paracetamol, NSAIDs, opioids, ergots, and oral triptans! * Verapamil - first line prevention * Lithium is also for prevention Prednisolone - short course to break the clusters

Question 162

Trigeminal neuralgia definition

Answer 162

severe unilateral pain in one or more branches of the trigeminal

Question 163

Trigeminal neuralgia epdmiology

Answer 163

* 0.003-0.3% a year * Rare in peope younger than 40 Femlaes more

Question 164

Trigeminal neuralgia risk factros

Answer 164

* Female * Age over 40 # Demylenating diseases (MS)

Question 165

Trigeminal neuralgia path

Answer 165

* 90% of patients have compression of a nerve by a vascular loop near the nerves root entry zone * Can also be causes by brainstem infarcts, posterioir fodda masses, demylenating diseases * Aberrant conduction alof the trigemincal nerve resulats in neuropathic pain Specific tiggers such as touch, washing, shaving, talking, cold weather, spicy food, caffine and citrus fruits can cases pain

Question 166

Trigeminal neuralgia key presintations

Answer 166

* Pain may be provoked by touch * Facial pain that can last between a few seconds and a few hours * Severe, with a trigeminal distribution * Unilateral * Electric shock sensation * Episodic * Provoked - cold/touch * Lacrimation * Facial swelling Ptosis

Question 167

Trigeminal neuralgia test

Answer 167

* Clinicla diagnosis MRI brain - if a sinister causes is suspected such as space occupying lesison

Question 168

Trigeminal neuralgia tx

Answer 168

* Carbamazepine - first line, dose is titrated unitll pain stops * Refer to neurology if it effects daily function Surgery - microvascuarl decompression or ablative surgery

Question 169

trigemnial neuralgia red flags

Answer 169

RED FLAGS * Onset before 40 * Pain in opthalamic division only * Sensory changes * Deafness * Histry of skin or oral lesison * Optic meuritis * Family history of MS

Question 170

epilepsy definition

Answer 170

Definition The recurrent tendency of spontaneous intermittent abnormal electrical activity in part of the brain, manifesting in seizures. It is caused by excessive, hypersynchronous neuronal discharge n the brain. Syncope - paroxysmal events whihc changes behaviours , sensation and cognitive process by insufficient blood/oxygen of the brain Paroxysmal - a sudden attack or increase in symptoms of a disease

Question 171

Epilepsy epidemiology

Answer 171

* 2% of UK. * Risk of having seizure in lifetime is 10% Most common in under 20 or over 60

Question 172

Epilepsy cases

Answer 172

Aetiology The neurons in the brain are synchronously active when they're not supposed to be. * Genetics - inhibition of GABA or more excitatory signals to be sent * Structural - visible neurological abnormalities that predispose to seizures * Metabolic - disorders can predispose

Question 173

Epilepsy RF

Answer 173

Risk Factors * Cerebrovascular damage * Head trauma * Cerebral infections * Family history * Premature birth * Congenital malformations of the brain * Dementia * Younger age * Infections

Question 174

Epilepsy path

Answer 174

Pathophysiology * Tonic - stiffening of the muscles * Atonic - the muscles relax too much * Clonic - convulsions and twitching * * The neurons send out loads of electrical discharges that are due to too much excitation/ too little inhibition * It can causes outward signs like jerking and convulsions, or inwards like fears and smells

Question 175

Epilepsy types of seizures

Answer 175

Types of seizures * Focal - limited to one hemisphere or lobe of the brain - affect hearing, speech, memory, emotions. These can be with or without impaired awareness. This is categorised into simple or complex. * Simple: no loss of consciousness, but sensory, autonomic, motor (jerking). These are also called auras are often pre-warnings of more. * Complex: focus of a larger area of eth brain and cases consciousness to be affected. Often in the temporal lobe, there will be post ictal confusion afterwards often. * Generalised - booth hemispheres of the brain are affected are subcategorised into tonic, atonic, clonic, tonic clonic, myoclonic and absence. * Tonic - stiffening of the muscles * Atonic - the muscles relax too much * Clonic - convulsions and twitching * Tonic-clonic - stiffening folowed by convulsions * Myoclonic - short muscle twitches whilst aware * Absence - imparied awareness/responsiveness - they become blank and stare into space Genralised seizures; affects bothe sides of the brain * Absence - rapid blingign and staring inot space * Tonic-clonic - cry out, loose consciousness, collapse, muscle jerks and spasms

Question 176

Epilepsy key presintations

Answer 176

Key presentations 4 phases - * Prodromal - confusion and modd disturbances * Early ictal - aura - warnding before hand such as sensory, cognitive or behavioural changes * Ictal - wil vary depeding on seizure types * Post ictal - confused, dowsy and irratiale dugin recovery (there can be todds palsy in this which is paralysis in arms and legs lasting 15 hours Epilepsy is considered to be a disease of the brain defined by any of the following conditions: * At least two unprovoked (or reflex) seizures occurring more than 24 hours apart * One unprovoked (or reflex) seizure and a probability of further seizures similar to the general recurrence risk (at least 60%) after two unprovoked seizures, occurring over the next 10 years * Diagnosis of an epilepsy syndrome. An epilepsy syndrome is a certain type of epilepsy characterised by its group of symptoms.

Question 177

Epilepsy test

Answer 177

1st line test * EEG - shows typical patterns in different forms of epilepsy * MRI brain - looks for structural problems * CT - look for structural problems * Arterial/venous blood gas - metabolic acidosis and raised lactate * ECG - exclude heart problems * Blood electrolytes - deranements can causes seizures * Blood cultures - spesis, encepalitis of meningitis * Inflamatory markers - if potential of infection

Question 178

Epilepsy differentail

Answer 178

Differential diagnosis * Anoxic seizures * Non epileptic seizures * Sleep releated conditions * Paroxysmal movement disorders * Migrane associated disorders

Question 179

Epilepsy tx

Answer 179

Treatment Generalised Tonic-Colonic seizures: * Sodium valporate/valporic acid - increased activity of GABA - tetrogenic, liver damage and hepatitis, hair loss and tremor * Carbamazepine - sodium channel blocker - anaplasitc aneamia and induced the p450 system so many prug interactions Focal: * Carbamzepine/lamotrigine * Second line - soudim valporate or levetircaetam Absence - * Sodium valproate * Epilepsy surgery to remove the causs of the seuizre - part of the brain/a tumour * Nerve stimulation - simulating the vagus neve to control seizures and release neurotransmitter * Keto diet

Question 180

Epilepsy complications

Answer 180

Complications * Status Epilepticus – if seizure lasts > 5 minutes, Ongoing or without returning to normal, Usually tonic clonic, Can be life-threating * Give thianie and B1 if evidance of alcohol abuse, then give benzodiazepine and levetiracetam/valproate

Question 181

what are non epileptic seizures

Answer 181

Non epileptic seizures * https://epilepsysociety.org.uk/about-epilepsy/what-epilepsy/non-epileptic-seizures * Seizures not due to epilepsy * Hypoglycemia, mentla pain, abuse, heart condition that causes fainting * Dissociative seizures- when it is caused by emotional factors such as after abuse. The emotion/memory is brought up and this leads to a seizure happening in order to stop thinkg aout it * NES will not show electiracl activity on an EEG * Treatet by psychotherapies and CBT `

Question 182

spinal cord compression definition

Answer 182

Definition * Compression of the arterires, veines, cerebrospinal fluid spaces and the cord.

Question 183

spinal cord compression epidemiology

Answer 183

Epidemiology 10-15% of cancer patients will develop metastasis that will affec the spinla cord

Question 184

spinal cord compression causes

Answer 184

Aetiology * Vertebral bod neoplasms - collapse or compression due to metastasis * Disk herniation - centrea has moved out though * Disc prolapse - there is a bulging * Infection - epidural abcess * Haematoma

Question 185

spinal cord compression key presintations

Answer 185

Key presentations * Acute or chronic onset depending on causes * Back pain that may precede weakness and secodnry loss * Weakness of legs * Sensory loss between 1-2 cord segments * UMN signs below lesion * LMN at level of lesion * L5-S1 lesion causes sciatica * L4-L5 -

Question 186

spinal cord compression test

Answer 186

1st line test * MRI is gold standard! Identifies that causes of compression * Biopsy/ surgical exploration * FBC, U&E, ESR * Xray to look for lung malignancy

Question 187

spinal cord compression differenetial

Answer 187

Differential diagnosis * Transverse myelitis * Multiple sclerosis * Carcinomatous meningitis * Cord vasculitis * Spinal artery thrombosis * Trauma * Guillian-barr syndrome

Question 188

spinal cord compression tx

Answer 188

Treatment * Epidural steroid injections * Surgical decompression - laminectomy (removal of lamina/spongy tissue between disk to relieve pressure) microdiscectomy - removal of herniated disc tissue * Steroids - dexamethasone * Radiotherapy if malignancy * Antibiotics if abscess

Question 189

what is sciatica

Answer 189

Sciatica * L5/S1 compression * Spinal causes: disk prolapse, spinal stenosis, disc herniation, sponylolithesis - vertebra becomes displaced * Non spinal - pirimormis surgery, pregnancy, trauma * Pain in buttock, back of thigh, leg, lateral aspect of little toe * Unilateral, weak plantar flexion, decreased sensation over lateral edge and sole of right foot * MRI and CT * Analgesia and surgical decompression

Question 190

Cauda equina syndrome definition

Answer 190

Definition * The cauda equina is formed at the nerve roots distal to the level of termination of the spinal cord at L1/L2 * Cauda equina syndrome is caused by damage to eth peripheral nerves at the cauda equina

Question 191

Cauda equina syndrome epidemiology

Answer 191

Epidemiology * Rare * Mainly in adults * Occurs in 2 % of herniated disks * Commonest causes is lumbar disk herniation at L4/L5 and L5/S1

Question 192

Cauda equina syndrome causes

Answer 192

Aetiology * Herniated disc (the most common cause) * Tumours, particularly metastasis * Spondylolisthesis (anterior displacement of a vertebra out of line with the one below). This will cause compression of the nerve root below seeing as the nerve root comes out above the disk * Abscess (infection) * Trauma

Question 193

Cauda equina syndrome path

Answer 193

Pathophysiology * There is compression of the cauda equina which causes the nerves to dysfunction (L3, L4, L5, S1, S2, S3, S4, S5 and Co). The cauda equina supply: * Sensation to the lower limbs, perineum, bladder and rectum * Motor innervation to the lower limbs and the anal and urethral sphincters * Parasympathetic innervation of the bladder and rectum

Question 194

Cauda equina syndrome key presintations

Answer 194

Key presentations Saddle anaesthesia (loss of sensation in the perineum – around the genitals and anus) Loss of sensation in the bladder and rectum (not knowing when they are full) Urinary retention or incontinence Faecal incontinence Bilateral sciatica Bilateral or severe motor weakness in the legs Reduced anal tone on PR examination Sexual dysfunction Areflexia - absence of deep tendon reflexes

Question 195

Cauda equina syndrome signs

Answer 195

Signs Areflexia Fasciculations Loss of bowel/bladder control Major difference between cauda equina and lesions higher up in the cord is that leg weakness is flaccid and areflexic (LMN lesion) and not spastic and hyperreflexia (UMN lesion)

Question 196

Cauda equina syndrome test

Answer 196

1st line test * MRI of the spine to confirm it * Examination - Knee flexion – test L5-S1 Ankle plantar flexion – test S1-S2 Straight leg raising – L5, S1 Femoral stretch test – L4

Question 197

Cauda equina syndrome differential

Answer 197

Differential diagnosis * Conus medullaris * Vertebral fracture * Peripheral neuropathy * Mechanical back pain

Question 198

Cauda equina syndrome tx

Answer 198

Treatment * Refer to neurosurgeon ASAP to relive pressure * Surgical decompression * High dose dexamethasone

Question 199

* 50-year-old nurse comes in with longstanding back pain and pain radiating down right leg to sole of right foot (SCIATICA – S1 LESION) * On examination there is weak plantar flexion, absent right ankle jerk, decreased sensation over lateral edge and sole of right foot * Where is lesion?

Answer 199

Right S1 root lesion due to disc prolapse placing pressure on root

Question 200

Motor neuron disease definition

Answer 200

Definition Motor neuorn diseases is an umbrella term for a variety of specific diagnossi, it is a cluster of degenerative diseases characterised by axonal degeneration f the euorsn in the motor cortex, cranial nerve nuculi and anteroir horn cells

Question 201

Motor neuron disease physiology

Answer 201

Physiology * Weakneess/paressi - imparied ability to move a body part in repsonse to will * Paralysis - ability to move a pody part in response to will is completlely lost * Ataxia - clumsy illdefined movement * Aoravia - disrder of consiocusly organised patterns of moevemnt * LMN - located in anteroir horns of the spinal cord and in cranil nerve nuculi in the brain stem * Alpha motor neuron = axon + skeletal muscle fibres it innovates + alpha motot rneuron * The mumber of musce fibres an almpha motot r neur inorvtes mena tahts it will be less finely controlled * UMN in the prefrontal gyrus, acxons travels down the croticospinal tract, lower motor neours sit in eh ventral horn of the spinal cord * * upper motor neuron damage - lesions is in eh cereberal hempsphere, cereberllum, brainstem or spinal cord. It cuases spaciticity and rigidity, hyperflexia of reflexes, increased tone, and no atrophy or fasciculations * Lower motor neours lesiosins causes weakness, atrophy, fasciculations and decreased reflexes and tone

Question 202

Motor neuron disease epidemiology

Answer 202

Epidemiology * Average onset is 60 * Males more * Fata in 2-4 years

Question 203

Motor neuron disease RF

Answer 203

Risk Factors * Age * Male * Family hisotry * Smoking * Exposure to heavy metals

Question 204

Motor neuron disease types

Answer 204

Types Amyotrophic laterla sclerosis: UMN+LMN * Familial form due to mutation in superoxide dismutase * Corticospinal tracts nd anrteri hotn cells are affected * Diseases stephen hawking had Progressive musclar atrophy: LMN * Muslce of talking and swallowing * Best prognosis Priayr lateral sclerosis: UMN * Least common, * Loss of betz cells in eth motor cortex Progressiev bulbar palsy :LMN * Affects supranuclear ad cranial nerves producing speech and swallow issues

Question 205

Motor neuron disease path

Answer 205

Pathophysiology * Upper and lower motor neuons stop functioning * There is a genetic componenet

Question 206

Motor neuron disease signs Signs

Answer 206

Signs Upper: * Increased tone * Hyper reflexes * Spacitcity Lower: * Reduced tone * Fasciculation (musle twistches) especially in toungue * Abesent reflexes * Atrophy of eth muscles Both: * Falls * Fatigue * Clumsiness * Prgressive wekaness Symptoms that shouldn’t occur: * Sensory problems * Extraocular invoelvement * Abdominal refelxes absent * Sphincer dysfunction

Question 207

Motor neuron disease test

Answer 207

1st line test * It is a clinical diagnosis - LMN % UMN in more than 3 regions is definite, in 2 regoins is probabale, it is also probabel with 1 and lab support and it is possible if there is only seigns in one region * Electromyography - evidance of fibrillation potentials * Nerve conduction studies - modest reductinos in amplitude * MRI of spine to rue out cerciacal cord compression and myelopathy * Lumbar puncture to exclude inflammatory causes

Question 208

Motor neuron disease differential

Answer 208

Differential diagnosis * Guillina barr * Spincla cord tuouts * Myasthenia gravis * Polyneuropathies * Ms

Question 209

Motor neuron disease treatment

Answer 209

Treatment * Riluzole- prolongs survival by 2-4 months bu protecting the motor neours form glutamate induced damage * Respiratory support -non invasive ventilation * Antispasmodic- baclofen * Analgesia * Feeling support * Speech and language therapy * End of life planning `

Question 210

Motor neuron disease complications and prognosis

Answer 210

Complications * Aspiration pneumonia * Resp failure Prognosis * Most patients die within 3 years * Mainly form Resp complications

Question 211

symtoms of an upper motor neuuron lesion

Answer 211

Spastic Hyperflexia Not present Yes yes No Cereberal hemisphere, cerebellum, brainstem, spinla cord

Question 212

symproms of a lower motor neuron lesion

Answer 212

Lower Flaccid Areflexia Present - especially in tongue Yes No Yes Anterori horn cell. Nerev roots, peripheral nerves, meuromusclar junction

Question 213

myasthenia gravis definition

Answer 213

Definition Autoimmune disease against nicotine ach receptors in the NMJ

Question 214

myasthenia gravisepidemiology

Answer 214

Epidemiology * Females * Peak onset for women is 30 and men is 60

Question 215

myasthenia gravis risk factors

Answer 215

Risk Factors * Oher autoimmune diseases * Thymic hyperplasia in 70% of cases and thymic tuour in 10%

Question 216

myasthenia gravis path

Answer 216

Pathophysiology * Type 2 hypersensitivity reaction where B cells produce anti Achr autoantibodes whihch interfere with the neuromuscular junctoin by bindging to nicotinic AChR on muscles cells * This measn that cnat respont to ach contract sinals and thsic causes muscle weakness as there are less receptors available * Activation of complemetn pathyway caues muscle cell destructon * Sime people produce muscle specific tryosine kinase aautoanitbodies which targets proteins in muscle cells

Question 217

myasthenia gravis signs

Answer 217

Signs * Muscle weakness Musce grous affected in order: * Extra occuar * Bulbar - weakness of jaw and chewing * Proximal limb * Face * Neck * Trunk *

Question 218

myasthenia gravis symptoms

Answer 218

Symptoms * Muscular fatigue * Muscle weakness * Ptosis * Diplopia - double vision * Bulbar - difficulty chewing and talking * Resp sificalties

Question 219

myasthenia gravis test

Answer 219

1st line test * Anti-AChR autoantibosies in serum (90% of cases) * Muscle specific kinase autoantibodies- 10% * Make them count to 50 outloud, their voice will get less and less audible * Arm outstretched and ask patient to look witjout moveing their head, after a while they eill be unable to keep the eyes raised * Nerve stimulation tests – show a characteristic decrement in evoked potential following stimulation of the motor nerve * Electromyography – fatiguability - ACh does NOT activate muscle cells properly resulting in weakness * CT/MRI of mediastinum – shows thymus hyperplasia, atrophy or tumour (thymoma)

Question 220

myasthenia gravis gold standard test

Answer 220

Gold standard test * Edrophonuium test - IV dose of edrophnium chloride to block actetylcholinesterase, this should reilve wekaness temporrily.

Question 221

myasthenia gravis tx

Answer 221

Treatment * 1st line – oral pyridostigmine (Acetylcholinesterase inhibitor) + prednisolone with azathioprine/methotrexate (immunosuppression)- Stops breakdown of ACh 🡪 increased concentrations of ACh * Give bisphosphonates as osteoporosis prophylaxis e.g. alendronate * Thymectomy – reduces muscle weakness * In myasthenia crises – give IV immunoglobulin and plasmapheresis * Rituximab - monoclonal antibod that targets b clls and reduced pridction of antibodies - available on NHS

Question 222

myasthenia gravis differnetiation

Answer 222

Differential diagnosis * Thyroid opthamology * MS * Myotonic dystophy * Briansem cranil nerve lesions * Lambert eaton syndrome

Question 223

myasthenia gravis complications

Answer 223

Complications * They can go into crisis and eh resp msucles stop working * They maey need oxygen mask and plasmapheresis

Question 224

lamb eaton syndrome definitino

Answer 224

Definition * Autoimmune disorder of the neuromusclar junction of the peripheral nerveour ssytyem * May occur as a paranoplastic disorer in association with cancer, normally small cell carcionma of the lung * Parenoplastic: immune system has a reaction to a toumour which causes destruciton of other normal tissues

Question 225

lamb eaton syndrome causes

Answer 225

Aetiology * Parenoplastic - small cell carcinoma * Autoimmune

Question 226

lamb eaton syndrome rf

Answer 226

Risk Factors * Autoimmune diseases - hashimotos, diabeties

Question 227

lamb eaton syndrome path

Answer 227

Pathophysiology * Antibodies target the voltage gated calcium channels at the presynaptic termials * This si maunly somatic nerves but can also effect the parasympathetic ones * This decreases the amount of working channels untill tehre is not enough calcium getting into the neuron n to causes it to release ACH * Similar to myasthenia gravis, but symptoms may improve with movement and its ore insidious

Question 228

lamb eaton syndrome key presintations

Answer 228

Key presentations * Slow development of symptoms * Gait difficulties before eye problems * Symetical proximal leg muscle weakness * Diplopia * Ptosis * Slurred speech * Dysphagia * Redued tendon reflexes (post tetanic potentiation - reflexes become normal again after stoonf muscle contraction for a while) Parasymathtic: * Dry mouth * Consipatino * Urinary problems * Impotente * Dizziness and faintin

Question 229

lamb eaton syndrome test

Answer 229

1st line test * Autoanntibodeies against voltage gates calcium channels * Electormyography - measure the electircal activity of muscles, lowerd amplitude, but this increases post exercise * Chest x ray - investigate for small cell carcinoma

Question 230

lamb eaton syndrome differential

Answer 230

Differential diagnosis * Botulism * Myasthenia gravis * Myopathy * Chronic inflammatory demyelinating neuropathy * Guillain Barr

Question 231

lamb eaton syndrome tx

Answer 231

Treatment * Manage underlying malignancy * Immunosuppressants - prednisolone * IV immunoglobulins - bind and neutralise autoantibodies * Plasmapheresis to get rid of the antibodies * Pyridostigmine/ amifampridine: allows more acetylcholine to be released in the neuromuscular junction synapses

Question 232

lamb eaton syndrome complications

Answer 232

Complications * Resp faliure * Osteoportiss form steroids * Aspriaion dur ot impared swallowing

Question 233

syncope definitino

Answer 233

Definition Temporarily loosing consciousness due to disruption of blood flow to the brain often leading to a fall. Presyncope: near loss of consciousness with light-headedness, muscular weakness, blurred vision, and feeling faint without actually fainting.

Question 234

syncope causes

Answer 234

Aetiology Primary * Reduced perfusion to the brain * Dehydration * Missed meals * Vasovagal resone to stimuli such as surprise, pain, blood Secondary * Hypoglycaemia * Anaemia * Hypovolemia * Infection * Anapylaxis * Arrhythmia * Valvular heart disease

Question 235

syncope RF

Answer 235

Risk Factors * Pregnant * Elderly * Vasoconstrictors * Alcohol abuse

Question 236

syncope path

Answer 236

Pathophysiology * A vasovagal episode is caused be a problem with the autonomic nervous system regulating blood flow to the brain * The parasympathetic NS is activated causing vasodilation, a drop in blood pressure and the person to faint

Question 237

syncope key presintations

Answer 237

Key presentations * Hot and clammy * Sweaty * Heavy * Dizzy or lightheaded * Vision blurry or dark * Headache * Unconsciousness

Question 238

syncope test

Answer 238

1st line test * A detailed history to find any triggers, head injury, neurologicla activitys, seizures, family history, heart problems. * ECG, echocardiogram, tilt table * Bloods to look for anaemia

Question 239

syncope differential

Answer 239

Differential diagnosis * Stroke * Seizure * Sleep disturbance * Accidental fall with head injury

Question 240

syncope tx

Answer 240

Treatment * Avoid dehydration * Eat well * Avoid standing still fo rtoo lomg * Rule out other pathology

Question 241

Carpel tunnel definition

Answer 241

Definition Carpal tunnel syndrome is a collection fo symptoms caused by compression of the median nerves in the carpal tunnel

Question 242

Carpel tunnel epidmiology

Answer 242

Epidemiology * Most common mononeuropathy and entrapment neuropathy * More common in females * Over 30 years

Question 243

Carpel tunnel causes

Answer 243

Aetiology * Compression/swelling * Repetitive stress (typing) * Obesity * Enforced flextion * Pregnancy * Rheumatoid arthritis * Myxoedema * Diabetic neuropathy * Neoplasms * Acromegally * Amyloidosis * Sarcoidosis

Question 244

Carpel tunnel path

Answer 244

Pathophysiology * Compression of the median nerve when there is inflammation of nearby tissues this means that the median nerves has to compete for space with 9 tendons and gets squished * This can start off as a dull ache/discomfort but often leads to paraesthesia * Thumb, index finger, middle finger, and any other skin innovated by the median nerve

Question 245

Carpel tunnel key presintations

Answer 245

Key presentations * Pain * Numbness * Paraesthesisa- burning and priiling sensation (should go away by hnging it over eth side of the bed and shaking it * Mucle weaness * Light touch, 2 point discrimination and sweating can all be impaired

Question 246

Carpel tunnel test

Answer 246

1st line test * Phalens manoeuvre - flex the wrist as far as possible and hold the position for a minute, this should causes numbness in median nerve inorvated areas * Tinels sign - tap the transvers carpal ligament to recreate feeling of pins and needles * Durkans test - manually compress the carpal tunnel for 30 seconds to causes carpel tunnel stndreom symptoms * Neurophysiology testing - confirm lesion site and severity as you can see slowing of the conduction velocity in the median sensory nerves

Question 247

Carpel tunnel tx

Answer 247

Treatment * Behavioural modification - using wrist supports , changing hand position when typing * Physical therapy * Non surgical - splinting or corticosteroid injections * Surgical - definitive management with decompression surgery - division of the transverse carpal ligament to open up the tunnel and relieve the pressure

Question 248

Wrist drop definition

Answer 248

A disorder cause by compressin o fteh radial nerve which innovates the extensor musces which causes thehand to drop.

Question 249

Wrist drop causes

Answer 249

* Stab wound * Lead poinsoning * Broken humerous * Sleeping on the nerve and compressing it (Saturday night and honeymooners palsy) * Dislocated shoulder improper correction

Question 250

Wrist drop key preintations

Answer 250

* Pain in wrist and hand * Weakness of wrist and fingers * Inability to straighten them out * Muscle shrinking * Numbness and tingling

Question 251

Wrist drop test

Answer 251

* Nerve conductio studies - * Hitchhikers sign - inabilito to extend thumb X rya or bone breakage

Question 252

Wrist drop tx

Answer 252

* Splintingo the wrist * Physiotherapy * Occupational therapy Surgical removal of bone sputs

Question 253

Claw hand causes

Answer 253

* Nerve * damage- ulnar, median, ulnar tunnel syndrome, cubital tunnel syndrome * Leprosy * Severe burns Compartment syndrome

Question 254

Claw hand risk factor

Answer 254

* Applying body weigth to push down a tool Polonged movemtn cuasing elbows to lead

Question 255

Claw hand path

Answer 255

* Complete - involves all digits of the hand - this is boh ulnar and median palsy Incomplete - only invvolves eh ilnar 2 digits

Question 256

Claw hand keyy presintations

Answer 256

* Muscle wasting * Mubmness * Inabilityto extrend IP joints * Upopposed actino fo extenosrs and the flexors digitorium Produdus as lumbrical of digits 4 and 5 are pralysed

Question 257

Claw hand test

Answer 257

* Electomyograph to look at uslce ans nerve functions * Nerev condution to check electrical signals

Question 258

Claw hand tx

Answer 258

* Splinting * Surgery * Tendon graft * Therapy to striaghten finger * Stengthening excerciss

Question 259

Food drop defintion

Answer 259

Difficulty lifting the front part of the foot causing it to drag on the ground when walking. This is mainly caused by peroneal nerve injury.

Question 260

Food drop causes

Answer 260

* Compression disorders -entrapment syndreoms * Traumatic injureis * Charcot marie toogh Stoke

Question 261

Food drop key presintation

Answer 261

oss of muscle control in the lower leg # * Muscle atrophy * Difficulty lifting foot and toes

Question 262

Food drop test

Answer 262

* imaging tests - x-rays, ultrasound, to look for compression or damage in legs, spinal cord and brain * Blood sugar test for diabetic neuropathy Electromyography

Question 263

Food drop tx

Answer 263

* Physical and occupational tehrapy * Braces, splintes and rthotics to help keep the ankle and foot in supported position Timie!!

Question 264

Mononueruotis multiplex nd polyneuropathy definiiont

Answer 264

Definition * Mononueruotis multiplex - a condition that effctes multiple nerves in no discernable pattern - the nerves have all been individualy damaged * Polyneuropathy -- many neves are damages, usually in symetical diseases

Question 265

peripheral neuropathy causes

Answer 265

Aetiology DAVID * Diabeties * Alcoholism * Vitamin deficiency (B12) * Infective/inherited (Guillain Barr, Charcot Marie - Toot) * Drugs - isoniazid

Question 266

peripheral neuropathy path

Answer 266

Pathophysiology * High glucose leves damage the small bloof vessles that supply nevres and stop oxygen and nutriens from finding the nerves * This leads to increaed function and death

Question 267

peripheral neuropathy key presintations

Answer 267

Key presentations * Numbness and tingling in feetor hands * Burning stabbing or shooting pains * Loss of balance and coordination * Muscle weakness - feet especially

Question 268

peripheral neuropathy tx

Answer 268

Treatment * Treat underlying casuse - diabeties * Neuropathic pain agents

Question 269

Brown-Sequard syndrome definition

Answer 269

Definition Hemisection of the spinal cord.

Question 270

Brown-Sequard syndrome causes

Answer 270

Aetiology * Space-occupying lesison * Intervertebral disc prolapse * Vertebral bone fractures * Trauma * Infections * MS

Question 271

Brown-Sequard syndrome path

Answer 271

Pathophysiology * Tract Action Decussation Corticospinal Moving all of the muscle Ipsilateral DCML Fine touch, vibraion, proprioception Ipsilateral Lateral spinothalamic Pain and temp Contralateral * Hemi section of the spinal cord damages the neural tracts causing a loss of pain, temp, touch and motor movement

Question 272

Brown-Sequard syndrome key presintations

Answer 272

Key presentations At the level of the lesion * ipsilateral spinothalamic tract dysfunction - loss of temp, pain and pressure. Below the level of the lesion * Ipsilateral corticospinal tract dysfunction (loss of motor) * Ipsilateral DCML (loss of proprioception, fine touch, 2 point discrimination) * Contralateral spinothalamic dysfunction - pain, temp, pressure

Question 273

Brown-Sequard syndrome test

Answer 273

1st line test MRI of spine

Question 274

Brown-Sequard syndrome treatment

Answer 274

Treatment Supportive - physical and occupational therapy Steroids - reduce swelling and inflammation

Question 275

Charcot-Marie-Tooth Syndrome definitino

Answer 275

Definition * A group of inherited diseases that affect the peripheral motor and sensory nerves

Question 276

Charcot-Marie-Tooth Syndrome path

Answer 276

Pathophysiology * Various types depending on different genetic mutation in the myelin sheath or axons * CMT1 and CMT2 are autosomal dominant diseases * CMT1 - caused by mutations in PMP22 and MPZ genes which encode protien got the myelin sheath this causes slowed impulse transmission, under a microscope there is onion bulb formation- axon is surrounded by new myelin overlaying older damaged myelin * CMT2 - caused by mutation in the MFN2 gene which codes for mitochondria leading to defective protein and disrupted neuronal death * These both cause muscle atrophy and when the sensory nerves are affected it affected the toes and feet ore as these are the longest nerves

Question 277

Charcot-Marie-Tooth Syndrome signs

Answer 277

Signs * Pes cavus - high foot arches * Hammer toes - middle joint to toe bends upwards * Mistal muscle wasting causing inverted champagne bottle legs * Claw hand caused by hand and arm muscle wasting * Thicked palpable nerves - common peroneal

Question 278

Charcot-Marie-Tooth Syndrome symptoms

Answer 278

Symptoms * Weakness in lower legs - loss of ankle dorsiflexion * Food drop * High stepped gait * Weakness in hands * Reduced tendon relfexes * Reduced muscle tone * Peripheral sensory loss * Tingling and burning sensation in hands and feet * Neuropathic pain

Question 279

Charcot-Marie-Tooth Syndrome test

Answer 279

1st line test * Nerve conduction studies - meaure ability of the nerevs to carry impulses * Neurologists and genetics to make diagnosis by lokng for mutations

Question 280

Charcot-Marie-Tooth Syndrome differential

Answer 280

Differential diagnosis * Diabttic neuropahy * Chronic inflamatory demylenatin polyneuropathy

Question 281

Charcot-Marie-Tooth Syndrome tx

Answer 281

Treatment * Physion * Occupational therapies * Podiatrists - help imporve foot symptoms nad get insoles and special shoews * Orthopaedic surgeons - correct disabiling joint deformaties

Question 282

Charcot-Marie-Tooth Syndrome complications

Answer 282

Complications * Osteoartheritis * Pain

Question 283

Duchenne Muscular Dystrophy definition

Answer 283

Definition Muscular dystrophy is a genetic condition that causes gradual weakening and wasting of the muscles

Question 284

Duchenne Muscular Dystrophy epidemiology

Answer 284

Epidemiology More common in males due to being x linked

Question 285

Duchenne Muscular Dystrophy path

Answer 285

Pathophysiology * Mutations in the dystrophin gene found on the xhornasome * Females are normally carriers * When the mutation is very sever ther eis no protien made at all, his si duchennes, this presents earlier and is more unpleasant * Mutations that lead to misshapen protnes lead to becker muscular dystrophy which is a much milder form of it * Dystophin protien links intracellular actin with another complex and link steh cytoskeleton actin and the extracellular matric helping ot stabalise the sarcomemma * Over time cratine kinase starts escaping and calcium leaks in and there is cell death * In the short term there is muscle regeneration leading to muscle fibers of different sizes but there is atrophy and wekenss overall

Question 286

Duchenne Muscular Dystrophy key presintations

Answer 286

Key presentations * 3-5 years age presintation * Weakness arouf pelvis * Child starts walking later thn average * Waddaling gate * Calf pseudohypertrophy - visibly enlarged calf'sdue to fat and fibrotic tissue moving in * Gowers sign - they have to push themselves up of the floor into downwards dog an then work there way up dur to muscle weakness

Question 287

Duchenne Muscular Dystrophy test

Answer 287

1st line test * High creatine kinase levels * Genetic testing - mutation in dystrophins gene * Muscle biopsy - staining for dystrophin * Electomyogram - distuinguish between neuropathic and myopatic pathology

Question 288

Duchenne Muscular Dystrophy tx

Answer 288

Treatment * Occupational therapy * Physio * Medice appliances- braces and wheelchair * Oral lsteroids - slow the process of muscle weakness * Creatine supplementation - give improvement in muscle strength * Genetic counselling - for patients who want ot have children * Surgery - spinal scoliosis and HF

Question 289

duchenne muscular dystrophy complications and prognosis

Answer 289

Complications * Resp failure * Scoliosis * Dilated cardiomyopathy and arrhythmias Prognosis Live to 25-35 years

Question 290

Depression definition

Answer 290

Definition Psychiatic - anxiety, alcohol abuse, substance misuse Physical - Parkinson's, MS, endocrine beta blockers, stroke, learning difficulties

Question 291

Depression definition

Answer 291

Definition Psychiatic - anxiety, alcohol abuse, substance misuse Physical - Parkinson's, MS, endocrine beta blockers, stroke, learning difficulties

Question 292

depression symotoms

Answer 292

Symptoms * Low mood * Loss of intrest * Loss of energy * Change in apetie * Sleep disturbances * Lack of concentration * Feeling of worthlesness * Innaporpruate guilt * Self harma nd suicide

Question 293

depression differntial

Answer 293

Differential diagnosis * Schizophreina * Dementia * Alcohol abus * Substance missuse

Question 294

deression tx

Answer 294

Treatment * Mental health crisis teams * CBT * Conselling * SSRIs # * Tricyclic antidepressants - amitriptyline and amoxamine * Infor and education

Question 295

primary brain tumours definitino

Answer 295

Definition Anaplastic - cancer cells that divide rapidly and have little ot no resemblance to normal cells

Question 296

primary brain tumours epidemiology

Answer 296

Epidemiology * 9th most common cancer * 55% are malignancy * Men under 45 and women under 35 * Secondary brain tumours are 10x more common than primary

Question 297

primary brain tumour types

Answer 297

Types * Gliomas - tumours of glial cells of spinal cord or brain, most will progress to be Glioblastoma Multiforme (GBM), there are three main types: * Glioblastoma multiforme - in cereberal hemisphere, - Histologically has pseudo-palisading pattern - peripheral tumour cells lined up around necrotic centre - Grade IV (most malignant) and worst outcome * Oligodendroglioma - 40-50s, frontal lobes of the cerberal cortex, slow growing tunours, small roud nuculi that look like fried eggs, * Ependyoma - ependymal cells (epitherium lining of the ventricels in the brain * Meningiomas - elderly and women, often benign, These tumours may also cause the formation of calcifications called psammoma bodies. * Pituitary tumours - benign, can press on optic chiasm, causes hormone problems, they are classed by the hormone released * Hemangioblastomas - blood vessel origins, often found I the cerebellum, slow glowing grade 1, this walled capillaries close to echoer * Acoustic neuroma -tumours of the Schwann cells surrounding the auditory nerve that innovates the inner ear. Slow glowing, can cause hearing loss, tinnitus, balance problems, facial nerve palsy

Question 298

brain tumour risk factors

Answer 298

Risk Factors * Affluent groups * Ionising radiation * Vinyl chloride * Genetics * #immunsurpression

Question 299

brain tumour path and types

Answer 299

Pathophysiology * Over 150 types * Meningioma - brain lining * Gliomas - intrinsic brain has mutates * Cranial nerve - schwannoma * Lymph cell tumours * Secondary - lung, breast, colorectal, testicular, renal, malignant melanoma * WHO classification - cell type, type I is most benign and IV is most malignant (most abnormal looking cells). Grade 1 is slow growing non malignant, 2 s cytologically atypical but slow growing, 3 is anaplastic and mitotic activity they are malignant, 4 is anaplasia, mitotic actitvity, microvascualr proliferation and necoriss. Thses are agressivly malignant * Classification 1: * Neuroepithelial tumours - astrocytes (most common), oligodendroglia, ependymal, neuroal, pineal, choroid plexus. Classification 2: * Cranial and spinal nerve: meningeal (second most common, lymphomas, germ cell tumours (elderly and immunosuppressed) * Metastatic tumours * Gliomas are are most common primary tumour and include astroyctes, oligodendrocytes and ependymal cells. astrocytes are the most common * Low grade tumour are slow growing and will have a longer survicval time * High grade - most common brain tumour, 85% of all new cases of malignant tumours. Survival is 3-5 years for III and 12 months for IV

Question 300

brain tumours key presintations

Answer 300

Key presentations Focal symtpms depending on area: * Temporal lobe - dysphasia & amnesia * Frontal lobe - hemiparesis, personality change, brocas dysphasia, astrogenesis * Parietal lobe - hemisensory loss, dysphasia, astrogenesis, reduction I 2 point discrimination * Occipital lobe - contralatera visula defects * Cerebellum - dysdiadochokinesis (impaired rapily alterating movement), ataxia, slurred speech, hypotonia, intention, tremor, nystagmus, gait abnormality (DASHING) Raised intracranial pressure: * Headache - in morning, worse when lying down, worse coughing, sneezing, derowsy * Vomiting * Altered mental state * Seizures * Visula field defects * Unilateral ptosis * 3 and 6 nerve palsy * Papilloedema * Hormone excess * Vestibular schwannoma- hearing loss, tinnitus, balance problems Low grade seizures often presnt with sizures and high grade wth rapily pregressing neurological defecit Secondary tumours: * Headache * Focal neurological signs * Ataxia * Fits * Nausea * Vomiting * Papilledema - a disc swelling is secondary to increased intracranial pressure The red flags are: * Headache PLUS * Ages over 50 * New/changed headache * Previous caner history * Headache with features of intercranial pressure increase - papilloedema and VI nerve palsy * New focal onset seizures * Rapidly progressing focal neurology * Past history of other cancers

Question 301

brain tumour test

Answer 301

1st line test * CT with contrast to look for tumours * MRI Molecular markers: * MGMT methylation - MGMT promoter methylation is the key mechanism of MGMT gene silencing and predicts a favorable outcome in patients with glioblastoma who are exposed to alkylating agent chemotherapy. * IDH 1 mutation - changes in these gene are asscaited with cncer growth * 1p19q co-deletion - short arm of chromossome 1 and the long arm of chromosome 19 which predictes a theraputic response to chemo and radiotherapy in pariens with gliomas (especially ologodendroglioma) * Tissue biopsy - to determine grade and guide management

Question 302

brain tumour differential

Answer 302

Differential diagnosis * Aneurisms * Abscess * Cyst * Haemorrhage * Idiopathic intracranial hypertension

Question 303

brain tumour tx

Answer 303

Treatment * Steroids - IV dexamethasone * Surgery - biopsy or resection * Chemotherapy - temozolamide, PCV * Radiotherapy - radical or palliative * Palliative care * Pituity tumour management - trans sphenoidal surgery, radiotherapy, bromocriptine, somatostatin analogues (octreotide)

Question 304

brain tumour complications and prognosis

Answer 304

Complications * Hydrocephalous - block CSF flow and cause hydrocephalous * Midline shift herniations through foreman magnum Prognosis Poor prognosis for secondary brain tumours.