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Neuro & Special Senses > Neurological Emergencies > Flashcards

Neurological Emergencies Flashcards

1
Q

Describe the clinical features of raised ICP? (9)

A
  • Headache
  • Altered mental state (lethargy, irritability, slow decision making, abnormal behaviour)
  • Papilloedma
  • Vomiting (progresses to projectile)
  • Pupil changes: irregular or dilated in one eye)
  • Cranial nerve palsies (esp unilateral ptosis, III or IV lesions)
  • Later changes: hemiparesis, raised BP, bradycardia
  • Seizures, syncope if acute rise in ICP
  • Cushings reflex
  • visual changes: black spots, blurring, enlarged blind spot and reduced peripheral vision (subacute) or reduced central vision and visual acuity (acute advanced)
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2
Q

Describe the headache of raised ICP

A

nocturnal, starting on waking, worse on coughing/ moving

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3
Q

Describe what papillodema looks like

A

blurring of disc margins, loss of venous pulsations, flame haemorrhages

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4
Q

What is the cushings reflex and why does it occur?

A

hypertension + bradycardia + low resp rate due to: Ischaemia at medulla causing sympathetic activation so rise in BP + tachycardia// Baroreceptors detect increase in BP causing Bradycardia// Ischemia @ pons/ medulla resp centers so low resp rate

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5
Q

How should raised ICP be investigated?

A
  • CT/ MRI for underlying lesions
  • blood glucose, renal function and osmolality
  • check for signs of CSF leak
  • ICP monitoring can be done
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6
Q

Give 6 causes of raised ICP

A
  • localised mass lesions (eg traumatic haematoma)
  • neoplasms (glioma, meningioma, mets)
  • abscesses
  • focal odema secondary to trauma, infection or infarction
  • disturbance of CSF circulation
  • major venous sinus thombosis/ obstruction
  • diffuse brain odema/ swelling
  • idiopathic intracranial hypertension
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7
Q

Give 5 causes of diffuse brain odema/ swelling

A
  • meningitis
  • encephalitis
  • diffuse brain injury
  • sub arachnoid haemorrhage
  • reyes syndrome
  • water intoxication
  • cerebral venous thrombosis
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8
Q

Describe the first line steps to management of raised ICP?

A
  • stabilise ABC
  • treat seizures with lorazepam +/- phenytoin
  • Head CT if meets criteria
  • assess C spine, immobilise and order neck CT if not cleared
  • involve neurosurgery
  • head elevation to 30 degrees
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9
Q

When should you intubate someone with a head injury/ raised ICP?

A 
If:
- sats <92%
or
- hypoxic on ABG 
or 
- GCS <8
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10
Q

Describe the further management of someone with raised ICP

A
  • Analgesia with morphine and sedation w/ propofol if necessary
  • mannitol (risk of hypovolaemia) or hypertonic saline if cerebral odema
  • barbiturate coma
  • hypothermia
  • decompressive craniotomy and shunts
  • treat cause (anticoag if venous outflow obstuction, diuretics then shunts if increased CSF, resections/ craniotomys/ steroids for SOLs)
  • hyperventilation (causes hypercapnic vasoconstriction so decreases ICP)
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11
Q

Describe the clinical features of a subarachnoid haemorrhage?

A
  • Sudden onset explosive headache (often occipital) lasting a few seconds or a fraction of a second then a diffuse headache which can last a week or so
  • almost always have N+V
  • altered mental status
  • seizures
  • neck stiffness/ meningism signs sometimes present around 6 hrs after
  • intraocular haemorrhages seen on fundoscopy in 15%
  • other signs of raised ICP
  • 10-15% die before getting to hospital
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12
Q

What warning symptoms may occur prior to SAH as aneurysm expands and bleeds slightly (sentinel bleeds)?

A
  • headache
  • dizziness
  • orbital pain
  • diplopia
  • ptosis
  • sensory or motor disturbance
  • seizures
  • dysphagia
  • bruits less common
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13
Q

Describe the investigation findings consistent with a subarachnoid haemorrhage? (4)

A
  • CT scan without contrast: hyperdense blood vessel in basal cisterns (98% sensitive after 2 hrs and 100% after 6, sensitivity drops after 24hrs)
  • cerebral panangiography then CT or MR angiography if aneurysm found
  • LP if CT scan negative but suspect SAH- spectrophotometry should be able to detect xanthochromia if SAH occured (detected from 12hrs- 2weeks after bleed)
  • ECG changes inc prolonged QT, Q waves, ST elevation
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14
Q

Describe the urgent and supportive management of a SAH? (4)

A
  • stabilise pt and send straight to neurosurgical unit +/- intubation, ventilation, NG tube, analgesia and antiemetics
  • endovascular obliteration by platinum spirals (coiling) or direct neurosurgical clipping to prevent rebleeding
  • oral nimodipine given to prevent vasospasm which leads to cerebral ischaemia/ stroke
  • hydrocephalus can occur as early or late complication, many will resolve on their own but some surgeons drain immediately
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15
Q

Describe the further management of an SAH? (3)

A
  • secondary prevention (stop smoking etc)
  • specialist rehab if lasting impairment
  • antifibrinolytics reduce rate of rebleeding but doesnt improve overall outcomes
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16
Q

Describe the clinical features of meningitis

A
  • Headache
  • Fever
  • Photophobia
  • Neck stiffness
  • Vomiting
  • Muscle pains
  • Non blanching purpuric rash
  • seizures
  • altered consciousness
  • Fatigue, muscle pain
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17
Q

What signs require urgent senior review +/- critical care input when managing a meningitis pt? (9)

A
  • rapidly progressive rash
  • poor peripheral perfusion (cap refill >4/ BP >90mmhg)
  • RR <8 or >30
  • HR <40 or >140
  • acidosis <7.3
  • WBC <4
  • lactate >4
  • GCS <12 or drop of 2
  • poor response to initial fluid resus
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18
Q

How should suspected meningitis (meningitis without signs of shock, severe sepsis or signs suggesting brain shift) be managed? (7)

A
  • blood cultures
  • bloods (FBC, renal function, glucose, lactate, clotting, viral PCR, blood gas)
  • LP
  • dexamethasone 10mg IV
  • ceftriaxone IV 2g
  • careful fluid resus
  • throat swab for meningococal culture
  • isolate until abx for 24 hrs, tell microbiology and PH
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19
Q

How should suspected meningitis with signs suggestive of brain shift/ raised ICP, severe sepsis or a rapidly evolving rash be managed? (9)

A
  • critical care input
  • secure airway, give O2
  • take bloods, do cultures
  • fluid resus (if shock/ sepsis/ rapidly evolving rash)
  • ceftriaxone 2g IV
  • Dexamethasone 10mg IV (omit if severe sepsis or rapdily evolving rash)
  • Neuro imagine such as CT head if signs of raised ICP
  • throat swab for meningococcal culture
  • DELAY LP
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20
Q

What tests should be done on CSF when meningitis suspected? (7)

A
  • glucose (w/ concurrent blood glucose)
  • protein
  • microscopy and culture
  • lactate
  • meningococcal and pneumococcal PCR
  • enteroviral, HSV, VZV PCR
  • consider investigations for TB meningitis
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21
Q

What are the criteria for delaying LP in meningitis?

A
  • signs of severe sepsis
  • rapidly evolving rash
  • severe cario/ resp compromise
  • significant bleeding rik
  • signs suggestive of brain compartment shift (do CT first): focal neurosigns, presence of papillodema, continious or uncontrolled seizures, GCS <12
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22
Q

State 5 complications of meningitis

A

septic shock, DIC, septic arthiritis, haemolytic anamia, pericadial effusion, subdural effusion, SIADH, seizures, hearing loss, cranial nerve dysfunction

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23
Q

Describe the clinical features of encephalitis (5)

A
  • bizarre behaviour or confusion
  • decreased GCS or coma
  • fever
  • headache
  • seizures
  • focal neuro signs (weakness, visual disturbance, aphasia, cerebellar signs)
  • history of travel or bite
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24
Q

Describe the key differences between meningitis and encephalitis?

A
  • Seizures uncommon in meningitis but common in encephalitis
  • photophobia, rash and neck stiffness much more common in meningitis
  • focal neurological signs are a hallmark feature of encephalitis, but only occur in some and later in meningitis
  • mental status is almost always altered in encephalitis, however is common but less so in meningitis
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25
Q

How should encephalitis be investigated?

A

How should encephalitis be investigated?

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26
Q

Give 3 common viral and 3 common non viral causes of encephalitis

A

Viral: HSV, arbovirus, EBV, CMv, VZV, HIB, mumps (paramyxo), measles, rabies, west nile
Non viral: any bacterial meningitis, lyme disease, TB, malaria, legionella, leptospirosis

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27
Q

How is encephalitis managed?

A
  • start aciclovir within 30 mins or arrival- 10mg/ kg/ 8hrs IV for 14 days as empirical treatment
  • specific therapies exist for CMV and toxoplasmosis
  • supportive therapy in HDU/ ITU if necessary
  • symptomatic treatment with phenytoin if necessary
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28
Q

Define status epilepticus

A

seizure lasting >30 mins or repeated seizures without intervening consciousness - usually in known epilepsy, if 1st presentation then high chance of structural brain lesion

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29
Q

How should status epilepticus be investigated/ assesed?

A
  • bedside glucose (dont miss this as cause) early
  • pulse oximetry and cardiac monitor while its happening
    After treatment started:
  • consider anticonvulsant levels, toxicology, LP, blood cultures, urine cultures, EEG, CT and carbon monoxide levels
  • CXR to evaluate for possible asipration
  • lab glucose, ABG, u&e, ca, fbc, ecg
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30
Q

Describe management of status epilepticus (from start of seizure) (inc paeds and adult doses)

A

0 mins: ABC, high flow O2, check BM, make surroundings safe- (50ml 50% dextrose if hypo)
5 mins: give IV lorazepam 0.1mg/ kg (4mg) slow bolus or rectal diazepam 10-20mg
10-15 mins: (if no response) give 2nd bolus
20-25 mins: phenytoin infusion 20mg/kg (up to 2g) at 50mg/min w/ ECG monitoring AND seek ITU help for general anaesthetic with propofol/ thiopentone if still going at 45 mins

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31
Q

Give 5 causes of spinal cord/ cauda equina compression?

A
  • neoplasms (breast, kindey, thyroid, lung, prostate mets, myeloma or primary bone tumours)
  • trauma
  • infections; abscesses
  • spinal stenosis
  • transverse myelitis
  • disc prolapses (rare but lumbar disc herniations typically cause CES)
  • post op haematoma
  • spondylolithesis
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32
Q

Describe the locations and functions of the 2 main ascending sensory tracts and the main motor tract within the spinal cord

A

Describe the locations and functions of the 2 main ascending sensory tracts and the main motor tract within the spinal cord

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33
Q

What are the upper motor neurone signs?

A
  • Weakness- esp of extensors in arms and flexors in legs
  • Hyperreflexia, clonus, upgoing planters
  • Hypertonia which is spastic (velocity dependent)- clasp knife
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34
Q

What are the lower motor neurone signs

A
  • weakness (pattern consistent with neuronal distribution)
  • muscle wasting
  • fasiculation
  • hypotonia/ flaccidity
  • reflexed reduced or absent
  • flexor planter reflex
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35
Q

Describe the type and distribution of motor and sensory deficit seen with cord lesions

A
  • usually bilateral motor deficit from below level of lesion down- initially LMN signs then UMN over the next hrs.
  • LMN signs + loss of reflexes at the level of the lesion
  • Presence of a sensory level
  • autonomic features may also be present & associated w/ worse prognosis (constipation, retention, incontinence)
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36
Q

Describe the MRC grading of muscle weakness

A 
0= no contraction
1= flicker of contraction 
2= some active movement
3= active movement against gravity
4= active movement against resistance
5= normal power (allowing for age)
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37
Q

Describe the classifications of head injuries?

A
  • Focal (slit into haematoma (sub, extra or intracerebral) or contusion (coup vs contracoup)
    vs
  • Diffuse (concussion vs diffuse axonal injury)
    AND
  • traumatic (split into open/ penetrating vs closed)
    vs
  • non traumatic (axonia, infection, CVA/ TIA, tumour etc)
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38
Q

Describe the pathophysiology of a concussion

A
  • Stretching of axons causes impaired neurotransmission, ion regulation and reduced blood flow causing temporary brain dysfunction
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39
Q

Describe the clinical features of post concusion syndrome

A

Difficulty thinking clearly, slowed down, confusion, headache, N+V, balance problems, tired, light sensitive, irritable, sad, sleep disturbance, trouble falling asleep

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40
Q

Describe the pathophys of diffuse axonal injury

A
  • Shearing of grey and white matter interface following traumatic acceleration/ deceleration or rotational forces
  • Leads to axonal death so cerebral odema so raised ICP and death
  • they get instate LOC with few recovering- v poor prognosis
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41
Q

State 5 signs of a basilar skull fracture

A

racoon eyes, CSF rhinorrhoea, CSF otorrhoea, battle sign, haemotympanum

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42
Q

Describe the differences in mechanism between extradural (EDH) and subdural (SDH) haemorrhage?

A

EDH: almost always traumatic
SDH: usually traumatic but less major trauma, can be spontaneous also

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43
Q

Describe the difference in presentation between EDH and SDH

A

EDH: young pt, LOC followed by lucid interval then rapid decline in consciousness, signs of raised ICP etc
SDH: acute bleeds can be any age, chronic bleeds seen in elderly, reduced GCS, neuro signs, or chronic bleeds= insidious neurological decline

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44
Q

Where is the bleed for EDH and SDH? What is the radiological appearance?

A

EDH: middle meningeal artery, lentiform shape, limited by suture lines
SDH: bridging veins, cresent shaped, not bound by suture lines but unable to cross midline due to falx cerebri, chronic bleeds appear hypodense- can have acute on chronic

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45
Q

What is the definitive management for EDH and SDH?

A

EDH: urgent craniotomy to relieve raised ICP, if small can just observe
SDH: acute- surgery to relieve raised ICP, if chronic and not causing symptoms then many are left alone

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46
Q

What are the criteria for a head CT within 1 hr of head injury?

A
  • GCS <13 or <15 after 2 hrs
  • focal neuro deficit
  • suspected skull or C spine fracture
  • seizure or vomiting >1 time
47
Q

What are the criteria for head CT within 8 hrs of head injury?

A 
- LOC or amnesia 
AND 
- age >65 (or)
- coagulopathy (or)
- high impact injury (or)
- retrograde amnesia of > 30 mins
48
Q

When is a CT neck NOT required to clear the neck and allow mobilisation?

A
  • no posterior midline cervical tenderness
  • no evidence of intoxication
  • pt altert and orientated to person, place, time and event
  • no focal neuro deficit
  • no painful distracting injuries
49
Q

How do acute bulbar and pseudobulbar palsies present differently?

A
  • A bulbar palsy is one of the nuclei of CN IX- XII (medulla)
  • A true bulbar palsy= LMN lesion (, flacid fassiculating tongue, normal or decreased jaw jerk and reduced gag reflex, quiet nasal speech)
  • corticobulbar palsy/ pseudobulbar palsy is UMN (hot potato speech, increased jaw and palatine reflexes, mood incontinent giggling/ weeping, spastic tongue)
50
Q

List causes of bulbar and a pseudobular palsies?

A

Bulbar: MND, guillian barre, polio, MG, syringobulbia, brainstem tumours or central pontine demyelinolysis
Pseudobulbar: MS, MND, BILATERAL stroke or centralpontine demyelinolysis

51
Q

Subarachnoid Haemorrhage is bleeding between the arachnoid and pia mater. What are the two broad causes? Give some specifics.

A

Traumatic - eg RTA (may be other cranial bleeds as well)

Spontaneous - Rupture of cerebral aneurysm, AV malformation, Vasculitis

52
Q

Give two modifiable and non modifiable risk factors for Subarachnoid Haemorrhage

A

Modifiable - Hypertension, Smoking

Non Modifiable - Female, ADPCKD

53
Q

Where are Berry Aneurysms normally located?

A

Located at branching points of major blood vessels (points of maximum haemodynamic stress)

30-40% ACA
25% PCA
20% MCA
10% Bifurcation

54
Q

Name four signs of Subarachnoid Haemorrhage

A

Neck Stiffness
Cranial Nerve Palsy
Reduced Consciousness
Diplopia

55
Q

When is a Lumbar Puncture for Subarachnoid Haemorrhage required?

A

If more than 6 hours from onset

If strong clinical suspicion but no findings on CT

56
Q

When should an LP be done for SAH? What would be a negative LP?

A

After 12 hours

If clear or if Oxyhaemaglobin alone (suggests trauma or traumatic tap)

57
Q

Name four findings you would expect from a positive Lumbar Puncture for SAH

A

Opening Pressure (elevated)
Red Cell Count (elevated)
Xanthochromia
Bilirubin

58
Q

Once an SAH has been diagnosed, what further investigation can be done?

A

CT Angiogram (to determine any underlying pathology, can be therapeutic - coil or clip at same time)

59
Q

Name four medical managements of SAH

A
  • IV fluids and monitoring
  • GCS<8 requires intubation
  • Nimodipine every 4h for 3w
  • Analgesia and Antiemetics to prevent ValSalva
60
Q

Name three possible surgical managements of SAH

A

Coiling
Clipping
External Ventricular Drain (if Hydrocephalus)

61
Q

Name three complications of SAH

A

Rebleeding
Vasospasm
Hydrocephalus

62
Q

Define Stroke

A

Clinical syndrome characterised by sudden onset of rapidly developing focal/global neurological disturbance, lasting more than 24h/leading to death (secondary to cerebral bloody supply disruption)

63
Q

Strokes can be either Ischaemic or Haemorrhagic. How can Ischaemic strokes be classified?

A

By the Bamford/Oxford Classification

TACS, PACS, LAC, POC

64
Q

Strokes can be either Ischaemic or Haemorrhagic. How can Haemorrhagic strokes be classified?

A

Intracerebral or Subarachnoid

65
Q

Describe the pathophysiology of an Ischaemic Stroke

A

Either due to Thrombosis, Embolism or Dissection

66
Q

Describe the pathophysiology of a Haemorrhagic Stroke

A

Usually due to Hypertension (but can also be due to vascular malformations, tumours, or bleeding disorders)

67
Q

Describe the TAC classification of Ischaemic Stroke

A

Unilateral Sensory/Motor Weakness
Homonymous Hemianopia
Higher Cerebral Dysfunction

Requires 3/3

68
Q

Describe the PAC classification of Ischaemic Stroke

A

Unilateral Sensory/Motor Weakness
Homonymous Hemianopia
Higher Cerebral Dysfunction

Requires 2/3

69
Q

Describe the LAC classification of Ischaemic Stroke

A

Can be:

Pure Sensory, Pure Motor, Sensorimotor, Ataxic

70
Q

Describe the POC classification of Ischaemic Stroke

A 
One of the following:
Brainstem Cerebellar Syndrome
Conjugate Eye Movement Disorder
Isolated Homonymous Hemianopia
Bilateral Sensorimotor Loss
Cranial Nerve Palsy and Contralateral Sensory/Motor
71
Q

Name two Posterior Stroke Syndromes

A

Locked In Syndrome - Basilar Artery

Wallenberg Syndrome - Posteroinferior Cerebellar Artery (Nystagmus, Vertigo, Horners, Diplopia, Dysphagia)

72
Q

FAST is the tool in the community used to screen for Stroke. What is the Hospital Tool called?

A

NIH Stroke Scale

  • Good Score is <4
  • Score>22 high risk of haemorrhagic transformation with thrombolysis
  • Score>26 means thrombolysis is contraindicated
73
Q

Name 5 investigations for a suspected stroke

A 
CT head
ECG
Echo
Bloods
Carotid Doppler
74
Q

How is a Haemorrhagic Stroke Managed?

A

Depends on the extent of the bleed and suitability for intervention

Large bleeds - decompressive hemicraniotomy or suboccipital craniotomy

75
Q

How is an Ischaemic Stroke managed ideally?

A

Thrombolysis with Alteplase (synthetic tPA)

If within 4.5 hours and NIHSS is between 5 and 26

76
Q

Name three contraindications to Thrombolysis

A

Ischaemic stroke within the past 3 months
Active Bleeding
Intracranial Neoplasm
Previous Haemorrhagic Stroke

77
Q

If Thrombolysis is contraindicated in terms of Ischaemic Stroke management, what is the next line?

A

300mg Asparin for 2w followed by 75mg Clopidogrel lifelong

78
Q

What is a Thrombectomy?

A

Removal of the thrombus done in specialist centres by interventional neuroradiology
Can be combined with Thrombolysis

Location specific and depends on brain tissue viability

79
Q

Name two early and two late complications of Stroke

A

Early - Haemorrhagic transformation, Cerebral Oedema (eg Malignant MCA)
Late - Mobility and Sensory Issues, Fatigue

80
Q

Raised ICP is initially compensated by shunting blood and CSF out. When it begins to decompensate, what are the symptoms?

A

Classic Triad - Headache (worse on waking), Papilloedema, Vomiting (projectile)

Pupillary changes, third nerve palsies, hypertension, bradycardia

81
Q

Name 5 first line managements for raised ICP

A 
Avoid Pyrexia
Head Elevation at 30 degrees
Sedation
Mannitol (not if hyperosmotic or hypovolaemic)
Analgesia
82
Q

Name three second line managements of raised ICP

A

Barbiturate Coma
Hypothermia
Decompressive Hemicraniectomy

83
Q

Name three complications of Status Epilepticus

A

Hyperthermia
Arrhythmia
Long term Neuro Damage

84
Q

What is the first line management for Meningitis at UHL?

A

IV Ceftriaxone (Meropenem if PA) and Dexamethasone (unless immunosupressed)

Notify PHE

85
Q

What is the first line management for Meningitis at UHL if over 60/immunocompromised?

A

Ceftriaxone + Amoxicillin + Dexamethasone

86
Q

Name 5 causes of Spinal Cord Injury

A 
Trauma
Tumours
Prolapsed Disc
Haematoma
Inflammatory DIsease
87
Q

Other than insiduous progression, name five red flags for spinal cord injury

A 
Gait Disturbance
Loss of Bladder/Bowel Function
L'hermitte's sign 
UMN signs in lower limbs
LMN signs in upper limbs
88
Q

How does a Spinal Cord Injury present?

A

Cervical Spine - Quadraplegia
Thoracic Spine - Paraplegia
Root pain in legs
May have loss of autonomic activity

89
Q

Define Cauda Equina

A

Compression of nerve roots caudal to the level of spinal cord termination, causing one or more of: Bladder/Bowel Dysfunction, Saddle Anaesthesia, Sexual Dysfunction, Lower Limb Neuro Deficit

90
Q

How can Cauda Equina be investigated?

A

Normally diagnosed from a good examination and history
MRI (40% show no abnormalities)
Urodynamic Studies (post surgery)

91
Q

Name two differentials for Cauda Equina

A

Conus Medullaris Syndrome (less prominent pain, more urinary retention and constipation)

Mechanical Back Pain

92
Q

How is Cauda Equina managed?

A

Urgent Surgical Decompression

Treat underlying cause

93
Q

What is Cerebral Perfusion Pressure?

A

The available blood for brain tissue

CPP = MAP - ICP

Aim for >90

94
Q

Describe a Subfalcine Herniation

A

Cingulate gyrus pushed under the free edge of the falx on the same side as mass
Can cause compression of the ACA

95
Q

Describe a Tentorial Herniation

A

Uncus herniates through Tentorial Notch

Damages ipsilateral CNIII

Occludes blood flow in Posterior Cerebral and Superior Cerebellar

Can cause secondary brain stem haemorrhage (Duret)

96
Q

Describe a Tonsilar Herniation

A

Cerebral Tonsils pushed through Foramen Magnum, compressing brainstem

97
Q

Name 5 worrying features following a Head Injury

A 
Vomiting
Reduced GCS
Confusion
Signs of a Basal Skull Fracture
Cushings triad
98
Q

What are the three branches of GCS?

A

Eye Opening
Verbal Response
Motor

Best response out of each side is used

99
Q

Describe the scoring of Eye Opening with GCS

A

4 - Spontaneously
3 - To Voice
2 - To Pain
1 - None

100
Q

Describe the scoring of Verbal Response with GCS

A 
5 - Conversation
4 - Confused
3 - Words
2 - Sounds
1 - None
101
Q

Describe the scoring of Motor Response with GCS

A 
6 - Obeys Commands
5 - Localises
4 - Withdraws
3 - Flexes
2 - Extends
1 - None
102
Q

Name four indicaions for Head CT post Head Injury according to NICE

A

GCS<13 initially
Suspected Skull #
Focal Neurological Signs
>1 episode of vomiting

103
Q

Describe the severity of Head Injury in terms of GCS

A

Mild (13-15)
Mod (9-12)
Severe (3-8)

104
Q

Name four broad classifications of Bulbar Palsies

A

Muscle Disorders
Diseases of Motor Nuclei in Medulla and Lower Pons
Diseases of Intramedullary Nerves of Spinal Cord
Diseases of Peripheral Nerves supplying muscles

105
Q

Name four presenting features of Bulbar Palsies

A

Weak and wasted tongue
Drooling
Absent palatal movements
Dysphonia

106
Q

Name five causes of Bulbar Palsy

A 
Diptheria
Poliomyelitis 
MND
Syringobulbia 
Guillaine Barre Syndrome
107
Q

What is Pseudobulbar Palsy?

A

Disease of the corticobulbar tracts causing an UMN lesion

May have UMN signs in limbs

108
Q

Name three causes of Pseudobulbar Palsy

A

MS
Internal Capsule Infarcts
Neurosyhphilis

109
Q

How is Bulbar Palsy investigated?

A

Speech Assessment (Electromagnetic Articulography)
Routine Bloods
CT/MRI

110
Q

How is Bulbar Palsy Managed?

A

Admission if dysphagia
Treat underling cause
Anticholinergics for drooling
Baclofen for Spasticity

111
Q

Name four diseases affecting the NMJ and causing Respiratory Distress

A

Lambert Eaton
Myasthenia Gravis
Clostrodium Botulinim
Organophosphates

112
Q

Name four diseases affecting the Muscle and causing Respiratory Distress

A

MND
Acid Maltase Deficiency
Electrolyte Disturbance (hypokalaemia)
Polymyositits

113
Q

Name one diseases affecting the nerves and causing Respiratory Distress

A

Guillaine Barre Syndrome

Neuro & Special Senses (12 decks)

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