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1
Q

TIA definition

A

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
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2
Q

TIA epidemiology

A

Epidemiology

  • 15% of first strokes are preceded by TIA
  • Male
  • Black ethnicity
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3
Q

TIA causes

A

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
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4
Q

TIA risk factors

A

Risk Factors

  • Age
  • Hypertension
  • Smoking
  • Diabetes
  • Heart disease - valvular ischemia, AF
  • TIA
  • Peripheral arterial disease
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5
Q

TIA pathophys

A

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
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6
Q

TIA symptoms

A

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
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7
Q

TIA test

A

1st line test

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

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8
Q

TIA scorning

A

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!!

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9
Q

TIA differential

A

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
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10
Q

TIA treatmtnet

A

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
    *
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11
Q

stroke definition

A

Stroke

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

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12
Q

stroke epidemiology

A
  • 68-75 is most common age
  • Male
    Asian and black African populations
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13
Q

stroke causes

A
  • 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
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14
Q

stroke path baed on region affected what symptoms will be presant

A
  • 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!!
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15
Q

stroke symtos

A
  • 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
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16
Q

stroke catogries

A

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
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17
Q

stroke tests

A

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

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18
Q

stroke differentials

A
  • Hypoglycemia
  • Hyponatremia
  • Uremia
  • Hypercalcema
  • Seizures
  • Tumours
    Complictated migrane
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19
Q

stroke treatment

A
  • 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

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20
Q

stroke prognosis

A

Totoal anteriro circulation stroke has wort outcomes!

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21
Q

Intracerebral haemorrage definition

A

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.

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22
Q

Intracerebral haemorrage causes

A

Aetiology

  • Hypertention
  • Atherlosclarosis
  • Vasculitis
  • Vascular tumours
  • Cerebral amylois angiopathy
  • Secondary to ischemaic stroke - blodd vessleis dead causing ti to rupture
  • Vasculitis
  • Tumours
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23
Q

Intracerebral haemorrage risk factors

A

Risk Factors

  • Head injury
  • Anyerisms
  • Ischeamic stokr
  • Anticoagulents such as warfrin
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24
Q

Intracerebral haemorrage path

A

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
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25
Q

Intracerebral haemorrage key presinstations

A

Key presentations

  • Headache
  • Weakness
  • Seizures
  • Vomiting
  • Reduced consciousness
  • Anterior or middle cerebral - numbness and muscle weakness
  • Broca - slurred speech
  • Posterior cerebral artery - vision disturbances
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26
Q

Intracerebral haemorrage test

A

1st line test

  • CT/MRI
  • Angiography
  • Check FBC and clotting
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27
Q

Intracerebral haemorrage treatment

A

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
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28
Q

Subarachnoid hemmorage most common presintation

A

Patient comes in with a thunderclap headache that really hurts.

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29
Q

Subarachnoid hemmorage causes

A
  • Trauma
  • Atraumatic cases
    Berry aneurisms (ommunicatinf and anterori arterys at crcle of willis
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30
Q

Subarachnoid hemmorage risk factors

A
  • Posy cystic kindye diseases
  • Coarctatino of the aorta
  • Ehler-Danlos/marfans
  • Increasing age
  • Smoking
  • Hypertension
  • Cocaine use
    Family history
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31
Q

Subarachnoid hemmorage pathophysiology

A

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

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32
Q

Subarachnoid hemmorage signs and symptoms

A
  • 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
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33
Q

Subarachnoid hemmorage tests

A
  • FBC
  • Serum glucose
  • Clotting screen
  • Urgent non contrast CT of the head
    ECG - look for arrhythmias, ischemia and ST elevation
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34
Q

Subarachnoid hemmorage treatment

A
  • 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
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35
Q

Extradural hemmorage most common presintations

A

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

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36
Q

Extradural hemmorage pathology

A
  • Head injury - fracture in temporal bone, laceration of middle menignela artery
    Blood accumulates rapidly over mins t hours between bone and dura
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37
Q

Extradural hemmorage key presintations

A
  • 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
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38
Q

Extradural hemmorage tests

A
  • CT scan - shows biconcave haematoma adjacent to skull
    Skull x-ray = may sow precure lines
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39
Q

Extradural hemmorage differential

A
  • Meningitis
  • Carotid dissection
  • Epilepsy
  • CO poisoning
    Subdural haemorrhage
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40
Q

Extradural hemmorage treatment

A
  • Refer to neurosurgeon
  • Burr hole craniotomy
  • Legation of bleeding vessel
  • Stabilise patient - ABCDE
    IV mannitol
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41
Q

subdural hemmorage common presintation

A

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

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42
Q

subdural hemmorage definition

A

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

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43
Q

subdural hemmorage epidemiology

A
  • Small brain - alcoholics or dementia
  • Shaken babies
    Elederly patients
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44
Q

subdural hemmorage causes

A
  • Contusions/lacerations
  • Base of skull fracture
  • Vertebral artery rupture/dissection
    Intravascular haemorrhage
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45
Q

subdural hemmorage risk factors

A
  • Traumatic head injury
  • Age
  • Alcoholics
    Shaken baby syndrome
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46
Q

subdural hemmorage path

A
  • 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
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47
Q

subdural hemmorage signs and symptoms

A
  • Personality change
  • Raised ICP
  • Herniatin
  • Vomiting
  • Headache
  • Fluctutaing levels of consciousness
  • Vomiting
  • Focal neurology, hemiparesis and sensory loss
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48
Q

subdural hemmorage

A
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49
Q

subdural heamorrage differential

A
  • Stroke
  • Dementia
  • CNS mass
    Subarachnoid haemorrhage
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50
Q

subdrual heamorrage treatment

A
  • Refer to neurosurgeon
  • Burr hole craniotomy and irrigation/removal of haematoma
  • Stabilise patient
  • IV mannitol to reduce ICP
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51
Q

what is teh eye thing with strokes

A
  • 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
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52
Q

Meningitis definition

A

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

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53
Q

Meningitis causes

A
  • 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

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54
Q

Meningitis risk factors

A
  • Immunocompramised (children and elderly, HIV, chemotherapy)
  • Non immunised - risk fo H.influenza, pnumococcla and meningiococcal
    Crowded enviroment - students in halls of residance
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55
Q

Meningitis path

A

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
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56
Q

Meningitis signs

A

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
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57
Q

Meningitis symotoms

A

Symptoms

  • Headache
  • Photophobia
  • Neck stiffness
  • Fever
  • N&V
  • Seizures
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58
Q

Meningitis test

A

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
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59
Q

Meningitis tx

A

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

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60
Q

Meningitis complications

A

Complications

  • Abscess
  • Cerebral oedema
  • Seizures
  • Memory loss
  • Cerebral palsy
  • Long term conative and behavioural deficit
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61
Q

Encephalitis definition

A

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

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62
Q

Encephalitis causes

A
  • Herpes simplex virus 1 and 32 (most common- 95%)
  • Varicalle zoster
  • Epstien barr
  • Cytomegaolivrus
  • HIV
  • Syphyliss
  • Tuberculois s
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63
Q

Encephalitis risk factors

A
  • HIV
  • Mosquito bite
  • Immunocompramsied
    Close contact with cats - toxoplasmosis
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64
Q

Encephalitis path

A
  • 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
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65
Q

Encephalitis signs and symptoms

A
  • 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
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66
Q

Encephalitis test

A
  • 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
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67
Q

Encephalitis treatment

A
  • Aciclovir to all
  • Gancicovit - HHV6 infection
  • A combination of ganciclovir and foscarnet is usually used in CMV
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68
Q

Encephalitis complications

A
  • Seizures stroke
  • Changes to memeory
  • Chronic pain
  • Learning disabilitys
  • Hormonla imbalance
  • Hydocephalous
  • Storke
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69
Q

MS definition

A

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.

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70
Q

MS epideimiology

A

Epidemiology

  • Women 2x as likely to get it
  • More common further from the equator - possible vit D link
  • 20-40 age of onset
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71
Q

MS RF

A

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
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72
Q

MS pathophysiology

A

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

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73
Q

MS key presintations

A

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)
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74
Q

MS types

A
  • 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
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75
Q

MS signs ans symptoms - there is a mnumonic

A

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
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76
Q

MS tests

A

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
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77
Q

MS differential

A

Differential diagnosis

  • Lupus
  • Sjorgrens
  • Polyarteritis nodosa
  • Lyme disease
  • Syphyliss
  • Aids
  • Cardiac embolic event
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78
Q

MS treatment

A

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

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79
Q

GBS definition

A

Definition

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

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80
Q

gbs epidemiology

A

Epidemiology

  • Males
  • 15-35 and 50-75
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81
Q

gbs causes

A

Aetiology

  • Campylobacter jejuni
  • EBV
  • Cytomegalovirus
  • HIV
  • Zoster
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82
Q

gbs path

A

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
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83
Q

gbs risk factors

A

Risk Factors

  • Resp or GI infection 3 weeks before onset
  • Vaccinatios
  • Post pregnancy
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84
Q

gbs signs and symptoms

A

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
    *
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85
Q

gbs test

A

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
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86
Q

gbs differential

A

Differential diagnosis

  • Hypokalaemia
  • Myasthenia gravis
  • Botulism
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87
Q

gbs treatment

A

Treatment

  • IV immunoglobulins
  • Plasma exchange
  • Supportive care
  • VTE prophylaxis- pulmonary embolism is leading cause of death)
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88
Q

gbs prognosis

A

Prognosis

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

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89
Q

Parkinsons definition

A

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

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90
Q

Parkinsons epidemiology

A

Epidemiology

Second most common neurodegenerative after Alzheimer’s
Male

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91
Q

Parkinsons risk factors

A

Risk Factors

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

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92
Q

Parkinsons path

A

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
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93
Q

Parkinsons key presintations

A

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
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94
Q

Parkinsons test

A

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
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95
Q

Parkinsons differential

A

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
* /

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96
Q

Parkinsons treatment

A

Treatment

  • Levodopa (DA precursor) and decarboxylase inhibitor -
  • /Monoamine oxidase B inhibitor(inhibit enzymatic breakdown of DA) - sleglinine, raseaglinein - stops breakdown of circulating dopamine
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97
Q

Parkinsons complications

A

Other notes

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

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98
Q

Huntington’s definition

A

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

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99
Q

Huntington’s epidemiology

A

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
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100
Q

Huntington’s causes

A

Aetiology

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

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101
Q

Huntington’s path

A

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.
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102
Q

Huntington’s key preintatino s

A

Key presentations

1st phase -
* Depression
* Incoordination
* Personality changes

2nd stage -
* Chorea - dance movements
* Abnormal eye movements
* Loss of coordination
* Dysphasia
* Dysarthria
* Dementia
* Depression
* Rigidity

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103
Q

Huntington’s test

A

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
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104
Q

Huntington’s differential

A

Differential diagnosis

  • Sydenhams choea - rheumatic fever
  • SLE
  • Basal ganglia stroke
  • Wilsons disease
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105
Q

Huntington’s treatment

A

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

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106
Q

alzheimers eipdeimology

A

Epidemiology

  • 50-75% of dementias
  • Females
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107
Q

alzheimers risk factors

A

Risk Factors

  • Age
  • Genetics
  • Cardiovascualr disease
  • Depression
  • Low education
  • Low socia suppirt
  • Head traumas
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108
Q

alzheimers path

A

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
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109
Q

alzheimers key presintations

A

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
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110
Q

alzheimers test

A

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
    *
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111
Q

alzheimers differential

A

Differential diagnosis

Other dementia
Depression
Delerium

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112
Q

alzheimers tx

A

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
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113
Q

Frontotemporal dementia definition

A

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

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114
Q

Frontotemporal dementia epidemiology

A
  • Makes up 2% of dementias
  • Affects patent at a younger age - 65
    Mena onset is 58
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115
Q

Frontotemporal causes

A

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

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116
Q

Frontotemporal dementia risk factors

A
  • 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
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117
Q

Frontotemporal dementia path

A
  • 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
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118
Q

Frontotemporal dementia key presintations

A

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

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119
Q

Frontotemporal dementia test

A
  • Cognitive assessment
  • MRI - shows changes in temporal and frontal lobes
    Brain biopsy after death
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120
Q

Frontotemporal dementia tx

A
  • Non pharmaceutical - exercise, physiotherapy, speech and language therapy, behaviour modification
    Pharmaceutical - SSRI, atypical antipsychotics
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121
Q

lewy body dementia definition

A

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

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122
Q

lewy body dementia risk factros

A
  • Older age
  • Male
    Family history
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123
Q

lewy body dementia pathophys

A
  • 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
124
Q

lewy body dementia key presintations

A

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

125
Q

lewy body dementia test

A
  • 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
126
Q

lewy body dementia tx

A
  • Domapine analouge - levodopa
    Cholinesterase inhibitors - donepezil incfreases ach availability
127
Q

vascular dementia definition

A

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

128
Q

vascular dementia epidemioloy

A
  • 20% of dementias
  • Often mixed with altzeimers
129
Q

vascular dementia causes

A
  • 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
130
Q

vascular dementia path

A
  • 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
131
Q

vascular dementia key presintaions

A
  • 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
131
Q

vascular dementia test

A
  • Neuropsycholoicgal test to asses function
  • Blood tests and examinations - ECG, virology, chets xrya
    CT/MRI to exclude other pathologies
132
Q

vascular dementia tx

A
  • No cure or medication
  • Manegement of RF - smoking, hgh BP< diabeties, cholesterol
  • Acetylcholinesterase inhibitors - in mixed dementia
    End of life care
133
Q

migrane definition

A

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.
134
Q

migrane epidemiology

A

Epidemiology

  • Most common causes of episodic headache
  • Females
135
Q

migrane causes

A

Aetiology

CHOCOLATE

* Chocolate 
* Hangovers 
* Orgasms 
* Cheese
* Oral contraceptives
* Lie-ins 
* Alcohol 
* Tummult - fluid noise 
* Exercise

Mensturation, red wine and bright lights as well

136
Q

migrane risk factors

A

Risk Factors

  • Family history
  • Female
  • Age
137
Q

migrane path

A

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
138
Q

migrane duagnosing types

A

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

139
Q

migrane test

A

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
140
Q

migrane differential

A

Differential diagnosis

  • Tension headache
  • Cluster headache
  • Medication overuse headache
  • Subarachnoid haemorrhage
  • Tumour
141
Q

migrane tx

A

Treatment

  • Avoid triggers
  • Acute attacks - mild NSAIDS/paracetamol/antiemetics
  • Prophylaxis - propranolol to topiramate (anticonvulsant)
  • Acupunctures
  • Amitriptylin (antidepressant)
  • Botulinum toxin type A -
142
Q

tension headache definition

A

Chronic daily, recurrent headaches. More of a dull ache

143
Q

tension headache epidemiology

A
  • Common primary headache
  • (<15 days/month) or chronic (>15 days a month for at least 3 month)
    Onset tends to be in the 20s
144
Q

tennsio headaceh causes

A

Neurovascular irritation which refers to scalp muscles and soft tissue

MD SCOLD
* Missed meals
* Conflict
* Stress
* Clenched jaw
* Overexertion
* Lack of sleep
Depression

145
Q

tension headache rf

A

Stress
Sleep deprivation
Bad posture
Hunger
Eyestrain
Anxiety
Noise

146
Q

tension headache path

A
  • 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
147
Q

tension headache diagnosis types

A
  • 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
148
Q

tension headache key presintations

A
  • Bilateral pressing/tight sensation
  • Nausea and vomiting
    Phonophobia and photophobia
149
Q

tension headache test

A
  • Patients is asked to keep a headache diary
  • CT or MRI of the head
    ESR to rule out giant cell arteriti
150
Q

tension headache differential

A
  • Migraine
  • Cluster headache
  • Giant cell arteritis
    Drug induced headache - wort when on analgesia such as opioids
151
Q

tension headache tx

A
  • 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
152
Q

cluster headache definition

A

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

153
Q

cluster headache epidemiology

A
  • Much rarer than mirage
  • Males more
  • 20-40 years
  • Smokers
154
Q

cluster headache causes

A
  • Autosomal dominant gene is involved
155
Q

cluster headache risk factors

A

Male
Smokers
Alcohol

156
Q

cluster headache path

A
  • 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
157
Q

cluster headache diagnosis tyes

A
  • 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
158
Q

cluster headache ke presintations

A

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

159
Q

cluster headache test

A
  • MRI /ct to rule out underlying cuases
    ESR - rle ot giant cell arteritis
160
Q

cluster headache differental

A
  • Migranes
  • Trigeminal automonim ceohalagias
  • Trauma
  • Idiopathic intercranial hypertension
  • Subarachnoid haemmore
  • Space occupying lesisons
  • Giant cell arteritis
  • Venous sinus thrombosis
    Malignant hypertension
161
Q

cluster headache tx

A
  • 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
162
Q

Trigeminal neuralgia definition

A

severe unilateral pain in one or more branches of the trigeminal

163
Q

Trigeminal neuralgia epdmiology

A
  • 0.003-0.3% a year
  • Rare in peope younger than 40
    Femlaes more
164
Q

Trigeminal neuralgia risk factros

A
  • Female
  • Age over 40 #
    Demylenating diseases (MS)
165
Q

Trigeminal neuralgia path

A
  • 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
166
Q

Trigeminal neuralgia key presintations

A
  • 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
167
Q

Trigeminal neuralgia test

A
  • Clinicla diagnosis
    MRI brain - if a sinister causes is suspected such as space occupying lesison
168
Q

Trigeminal neuralgia tx

A
  • Carbamazepine - first line, dose is titrated unitll pain stops
  • Refer to neurology if it effects daily function
    Surgery - microvascuarl decompression or ablative surgery
169
Q

trigemnial neuralgia red flags

A

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
170
Q

epilepsy definition

A

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

171
Q

Epilepsy epidemiology

A
  • 2% of UK.
  • Risk of having seizure in lifetime is 10%
    Most common in under 20 or over 60
172
Q

Epilepsy cases

A

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
173
Q

Epilepsy RF

A

Risk Factors

  • Cerebrovascular damage
  • Head trauma
  • Cerebral infections
  • Family history
  • Premature birth
  • Congenital malformations of the brain
  • Dementia
  • Younger age
  • Infections
174
Q

Epilepsy path

A

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
175
Q

Epilepsy types of seizures

A

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

176
Q

Epilepsy key presintations

A

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.

177
Q

Epilepsy test

A

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
178
Q

Epilepsy differentail

A

Differential diagnosis

  • Anoxic seizures
  • Non epileptic seizures
  • Sleep releated conditions
  • Paroxysmal movement disorders
  • Migrane associated disorders
179
Q

Epilepsy tx

A

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
180
Q

Epilepsy complications

A

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
181
Q

what are non epileptic seizures

A

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
    `
182
Q

spinal cord compression definition

A

Definition

  • Compression of the arterires, veines, cerebrospinal fluid spaces and the cord.
183
Q

spinal cord compression epidemiology

A

Epidemiology

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

184
Q

spinal cord compression causes

A

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
185
Q

spinal cord compression key presintations

A

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 -
186
Q

spinal cord compression test

A

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
187
Q

spinal cord compression differenetial

A

Differential diagnosis

  • Transverse myelitis
  • Multiple sclerosis
  • Carcinomatous meningitis
  • Cord vasculitis
  • Spinal artery thrombosis
  • Trauma
  • Guillian-barr syndrome
188
Q

spinal cord compression tx

A

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
189
Q

what is sciatica

A

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
190
Q

Cauda equina syndrome definition

A

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
191
Q

Cauda equina syndrome epidemiology

A

Epidemiology

  • Rare
  • Mainly in adults
  • Occurs in 2 % of herniated disks
  • Commonest causes is lumbar disk herniation at L4/L5 and L5/S1
192
Q

Cauda equina syndrome causes

A

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
193
Q

Cauda equina syndrome path

A

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

194
Q

Cauda equina syndrome key presintations

A

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

195
Q

Cauda equina syndrome signs

A

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)

196
Q

Cauda equina syndrome test

A

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
197
Q

Cauda equina syndrome differential

A

Differential diagnosis

  • Conus medullaris
  • Vertebral fracture
  • Peripheral neuropathy
  • Mechanical back pain
198
Q

Cauda equina syndrome tx

A

Treatment

  • Refer to neurosurgeon ASAP to relive pressure
  • Surgical decompression
  • High dose dexamethasone
199
Q
  • 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?
A

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

200
Q

Motor neuron disease definition

A

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

201
Q

Motor neuron disease physiology

A

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
202
Q

Motor neuron disease epidemiology

A

Epidemiology

  • Average onset is 60
  • Males more
  • Fata in 2-4 years
203
Q

Motor neuron disease RF

A

Risk Factors

  • Age
  • Male
  • Family hisotry
  • Smoking
  • Exposure to heavy metals
204
Q

Motor neuron disease types

A

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
205
Q

Motor neuron disease path

A

Pathophysiology

  • Upper and lower motor neuons stop functioning
  • There is a genetic componenet
206
Q

Motor neuron disease signs Signs

A

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

207
Q

Motor neuron disease test

A

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
208
Q

Motor neuron disease differential

A

Differential diagnosis

  • Guillina barr
  • Spincla cord tuouts
  • Myasthenia gravis
  • Polyneuropathies
  • Ms
209
Q

Motor neuron disease treatment

A

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
    `
210
Q

Motor neuron disease complications and prognosis

A

Complications

  • Aspiration pneumonia
  • Resp failure

Prognosis

  • Most patients die within 3 years
  • Mainly form Resp complications
211
Q

symtoms of an upper motor neuuron lesion

A

Spastic

Hyperflexia

Not present

Yes

yes

No

Cereberal hemisphere, cerebellum, brainstem, spinla cord

212
Q

symproms of a lower motor neuron lesion

A

Lower

Flaccid

Areflexia

Present - especially in tongue

Yes

No

Yes

Anterori horn cell. Nerev roots, peripheral nerves, meuromusclar junction

213
Q

myasthenia gravis definition

A

Definition

Autoimmune disease against nicotine ach receptors in the NMJ

214
Q

myasthenia gravisepidemiology

A

Epidemiology

  • Females
  • Peak onset for women is 30 and men is 60
215
Q

myasthenia gravis risk factors

A

Risk Factors

  • Oher autoimmune diseases
  • Thymic hyperplasia in 70% of cases and thymic tuour in 10%
216
Q

myasthenia gravis path

A

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
217
Q

myasthenia gravis signs

A

Signs

  • Muscle weakness

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

218
Q

myasthenia gravis symptoms

A

Symptoms

  • Muscular fatigue
  • Muscle weakness
  • Ptosis
  • Diplopia - double vision
  • Bulbar - difficulty chewing and talking
  • Resp sificalties
219
Q

myasthenia gravis test

A

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)
220
Q

myasthenia gravis gold standard test

A

Gold standard test

  • Edrophonuium test - IV dose of edrophnium chloride to block actetylcholinesterase, this should reilve wekaness temporrily.
221
Q

myasthenia gravis tx

A

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
222
Q

myasthenia gravis differnetiation

A

Differential diagnosis

  • Thyroid opthamology
  • MS
  • Myotonic dystophy
  • Briansem cranil nerve lesions
  • Lambert eaton syndrome
223
Q

myasthenia gravis complications

A

Complications

  • They can go into crisis and eh resp msucles stop working
  • They maey need oxygen mask and plasmapheresis
224
Q

lamb eaton syndrome definitino

A

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
225
Q

lamb eaton syndrome causes

A

Aetiology

  • Parenoplastic - small cell carcinoma
  • Autoimmune
226
Q

lamb eaton syndrome rf

A

Risk Factors

  • Autoimmune diseases - hashimotos, diabeties
227
Q

lamb eaton syndrome path

A

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
228
Q

lamb eaton syndrome key presintations

A

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

229
Q

lamb eaton syndrome test

A

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
230
Q

lamb eaton syndrome differential

A

Differential diagnosis

  • Botulism
  • Myasthenia gravis
  • Myopathy
  • Chronic inflammatory demyelinating neuropathy
  • Guillain Barr
231
Q

lamb eaton syndrome tx

A

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
232
Q

lamb eaton syndrome complications

A

Complications

  • Resp faliure
  • Osteoportiss form steroids
  • Aspriaion dur ot impared swallowing
233
Q

syncope definitino

A

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.

234
Q

syncope causes

A

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

235
Q

syncope RF

A

Risk Factors

  • Pregnant
  • Elderly
  • Vasoconstrictors
  • Alcohol abuse
236
Q

syncope path

A

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
237
Q

syncope key presintations

A

Key presentations

  • Hot and clammy
  • Sweaty
  • Heavy
  • Dizzy or lightheaded
  • Vision blurry or dark
  • Headache
  • Unconsciousness
238
Q

syncope test

A

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
239
Q

syncope differential

A

Differential diagnosis

  • Stroke
  • Seizure
  • Sleep disturbance
  • Accidental fall with head injury
240
Q

syncope tx

A

Treatment

  • Avoid dehydration
  • Eat well
  • Avoid standing still fo rtoo lomg
  • Rule out other pathology
241
Q

Carpel tunnel definition

A

Definition

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

242
Q

Carpel tunnel epidmiology

A

Epidemiology

  • Most common mononeuropathy and entrapment neuropathy
  • More common in females
  • Over 30 years
243
Q

Carpel tunnel causes

A

Aetiology

  • Compression/swelling
  • Repetitive stress (typing)
  • Obesity
  • Enforced flextion
  • Pregnancy
  • Rheumatoid arthritis
  • Myxoedema
  • Diabetic neuropathy
  • Neoplasms
  • Acromegally
  • Amyloidosis
  • Sarcoidosis
244
Q

Carpel tunnel path

A

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
245
Q

Carpel tunnel key presintations

A

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
246
Q

Carpel tunnel test

A

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
247
Q

Carpel tunnel tx

A

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
248
Q

Wrist drop definition

A

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

249
Q

Wrist drop causes

A
  • Stab wound
  • Lead poinsoning
  • Broken humerous
  • Sleeping on the nerve and compressing it (Saturday night and honeymooners palsy)
  • Dislocated shoulder improper correction
250
Q

Wrist drop key preintations

A
  • Pain in wrist and hand
  • Weakness of wrist and fingers
  • Inability to straighten them out
  • Muscle shrinking
  • Numbness and tingling
251
Q

Wrist drop test

A
  • Nerve conductio studies -
  • Hitchhikers sign - inabilito to extend thumb
    X rya or bone breakage
252
Q

Wrist drop tx

A
  • Splintingo the wrist
  • Physiotherapy
  • Occupational therapy
    Surgical removal of bone sputs
253
Q

Claw hand causes

A
  • Nerve
  • damage- ulnar, median, ulnar tunnel syndrome, cubital tunnel syndrome
  • Leprosy
  • Severe burns
    Compartment syndrome
254
Q

Claw hand risk factor

A
  • Applying body weigth to push down a tool
    Polonged movemtn cuasing elbows to lead
255
Q

Claw hand path

A
  • Complete - involves all digits of the hand - this is boh ulnar and median palsy
    Incomplete - only invvolves eh ilnar 2 digits
256
Q

Claw hand keyy presintations

A
  • 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
257
Q

Claw hand test

A
  • Electomyograph to look at uslce ans nerve functions
  • Nerev condution to check electrical signals
258
Q

Claw hand tx

A
  • Splinting
  • Surgery
  • Tendon graft
  • Therapy to striaghten finger
  • Stengthening excerciss
259
Q

Food drop defintion

A

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.

260
Q

Food drop causes

A
  • Compression disorders -entrapment syndreoms
  • Traumatic injureis
  • Charcot marie toogh
    Stoke
261
Q

Food drop key presintation

A

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

262
Q

Food drop test

A
  • imaging tests - x-rays, ultrasound, to look for compression or damage in legs, spinal cord and brain
  • Blood sugar test for diabetic neuropathy
    Electromyography
263
Q

Food drop tx

A
  • Physical and occupational tehrapy
  • Braces, splintes and rthotics to help keep the ankle and foot in supported position
    Timie!!
264
Q

Mononueruotis multiplex nd polyneuropathy definiiont

A

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
265
Q

peripheral neuropathy causes

A

Aetiology

DAVID

* Diabeties 
* Alcoholism 
* Vitamin deficiency (B12) 
* Infective/inherited (Guillain Barr, Charcot Marie - Toot)
* Drugs - isoniazid
266
Q

peripheral neuropathy path

A

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
267
Q

peripheral neuropathy key presintations

A

Key presentations

  • Numbness and tingling in feetor hands
  • Burning stabbing or shooting pains
  • Loss of balance and coordination
  • Muscle weakness - feet especially
268
Q

peripheral neuropathy tx

A

Treatment

  • Treat underlying casuse - diabeties
  • Neuropathic pain agents
269
Q

Brown-Sequard syndrome definition

A

Definition

Hemisection of the spinal cord.

270
Q

Brown-Sequard syndrome causes

A

Aetiology

  • Space-occupying lesison
  • Intervertebral disc prolapse
  • Vertebral bone fractures
  • Trauma
  • Infections
  • MS
271
Q

Brown-Sequard syndrome path

A

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
272
Q

Brown-Sequard syndrome key presintations

A

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

273
Q

Brown-Sequard syndrome test

A

1st line test

MRI of spine

274
Q

Brown-Sequard syndrome treatment

A

Treatment

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

275
Q

Charcot-Marie-Tooth Syndrome definitino

A

Definition

  • A group of inherited diseases that affect the peripheral motor and sensory nerves
276
Q

Charcot-Marie-Tooth Syndrome path

A

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
277
Q

Charcot-Marie-Tooth Syndrome signs

A

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
278
Q

Charcot-Marie-Tooth Syndrome symptoms

A

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
279
Q

Charcot-Marie-Tooth Syndrome test

A

1st line test

  • Nerve conduction studies - meaure ability of the nerevs to carry impulses
  • Neurologists and genetics to make diagnosis by lokng for mutations
280
Q

Charcot-Marie-Tooth Syndrome differential

A

Differential diagnosis

  • Diabttic neuropahy
  • Chronic inflamatory demylenatin polyneuropathy
281
Q

Charcot-Marie-Tooth Syndrome tx

A

Treatment

  • Physion
  • Occupational therapies
  • Podiatrists - help imporve foot symptoms nad get insoles and special shoews
  • Orthopaedic surgeons - correct disabiling joint deformaties
282
Q

Charcot-Marie-Tooth Syndrome complications

A

Complications

  • Osteoartheritis
  • Pain
283
Q

Duchenne Muscular Dystrophy definition

A

Definition

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

284
Q

Duchenne Muscular Dystrophy epidemiology

A

Epidemiology

More common in males due to being x linked

285
Q

Duchenne Muscular Dystrophy path

A

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
286
Q

Duchenne Muscular Dystrophy key presintations

A

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
287
Q

Duchenne Muscular Dystrophy test

A

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
288
Q

Duchenne Muscular Dystrophy tx

A

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
289
Q

duchenne muscular dystrophy complications and prognosis

A

Complications

  • Resp failure
  • Scoliosis
  • Dilated cardiomyopathy and arrhythmias

Prognosis

Live to 25-35 years

290
Q

Depression definition

A

Definition

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

291
Q

Depression definition

A

Definition

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

292
Q

depression symotoms

A

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
293
Q

depression differntial

A

Differential diagnosis

  • Schizophreina
  • Dementia
  • Alcohol abus
  • Substance missuse
294
Q

deression tx

A

Treatment

  • Mental health crisis teams
  • CBT
  • Conselling
  • SSRIs #
  • Tricyclic antidepressants - amitriptyline and amoxamine
  • Infor and education
295
Q

primary brain tumours definitino

A

Definition

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

296
Q

primary brain tumours epidemiology

A

Epidemiology

  • 9th most common cancer
  • 55% are malignancy
  • Men under 45 and women under 35
  • Secondary brain tumours are 10x more common than primary
297
Q

primary brain tumour types

A

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
298
Q

brain tumour risk factors

A

Risk Factors

  • Affluent groups
  • Ionising radiation
  • Vinyl chloride
  • Genetics
  • # immunsurpression
299
Q

brain tumour path and types

A

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
300
Q

brain tumours key presintations

A

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
301
Q

brain tumour test

A

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
302
Q

brain tumour differential

A

Differential diagnosis

  • Aneurisms
  • Abscess
  • Cyst
  • Haemorrhage
  • Idiopathic intracranial hypertension
303
Q

brain tumour tx

A

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)
304
Q

brain tumour complications and prognosis

A

Complications

  • Hydrocephalous - block CSF flow and cause hydrocephalous
  • Midline shift herniations through foreman magnum

Prognosis

Poor prognosis for secondary brain tumours.

Phase 2a (18 decks)

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