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REVISION BDS > neurology p237 > Flashcards

neurology p237 Flashcards

1
Q

astrocytes

A

regulate transmission of signals in the brain

provide nutrients

create the blood brain barrier along with endothelial cells

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2
Q

microglia

A

act as housekeepers in the nervous system, dealing with waste and pathogens

antigen presentation

cytotoxicity

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3
Q

ependymal cells

A

line the ventricles of the brain and central canal of the spinal cord

produce CSF

role in neuroregeneration when damaged

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4
Q

Schwann cells

A

provide myelination to axons in PNS

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5
Q

oligodendrocytes

A

provide myelination to axons in CNS

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6
Q

Peripheral nervous system

types of sensory neurons 4

A

Aα - Myelinated, very large diameter
Aβ - Myelinated, large diameter
Aδ - Myelinated, small diameter
C - Unmyelinated, small diameter

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7
Q

peripheral nerve roles

A

carry information to and from the CNS

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8
Q

afferent (sensory) nerves

A

➡Carry information to the CNS
➡Afferent signals in somatic nerves are associated with
sensations/perceptions
➡afferent signals from internal organs (‘viscera’) do not usually give rise to sensations

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9
Q

efferent (motor) nerves

A

➡Carry information away from the CNS
➡Cause actions: muscle contractions, etc
➡‘somatic’ efferents control voluntary muscle
➡‘visceral’ efferents constitute the autonomic nervous system

  • the ANS controls smooth and cardiac muscle and some glands
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10
Q

central nervous system comprises

A

brain and spinal cord

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11
Q

brain

A

perceives and processes sensory stimuli

executes voluntray motor responses through skeletal muscle

regulates hoemostatic mechanisms (autonomic)

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12
Q

spinal cord

A

initiates reflexes from ventral horn and lateral horn grey matter

pathways for sensory and motor fucntions between periphery and brain

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13
Q

white matter

A

consists of axons and oligodendrocytes (the myelination of the latter gives its dark appearance)

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14
Q

grey matter

A

contains neurons and unmyelinated fibres

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15
Q

autonomic nervous system

A

hypothalamis controls ANS activity

subconcious cerbral input via limbic system

spinal cord too

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16
Q

stroke

A

acute focal neuro deficit resulting from cerbrovascular disease and lasting more than 24hrs or causing early death - if less than 24hors then it is deemed a TIA

either infarct or haemorrhagic

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17
Q

Transiet ischaemic attack caused

A

ususally by platelet bound embolus, which is broken down and person returns to normal

brain has no resistance to pressure in life so expands into cranial spaces

there is little collateral arterial supply in the brain so the affected brain area will die off

incidences of past TIA in stroke is 25%

lower cerebral vessels usually have anastamses but there is more difficulties when there is upper vessels

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18
Q

types of stroke

A

total anterior circulation stroke

partial anterior ciculation stroke

lacunar stroke

posterior ciruclation stroke

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19
Q

total anteiror circulation stroke

A

occlsaion of middle cerebral artery

effects majority of anterior part of one cerebral hemisphere

causes contralateral impairments affecting movements

  • hemiparesis/hemianaesthesia
  • homonyous hemianopia - some half of vision gone in both eyes
  • higher functions diminish - speech so dyspraxia
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20
Q

partial anterior circulation stroke

A

not as severe as total

doesn’t have the higher cerebral function involvement

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21
Q

lacunar stroke

A

small stroke with limited deficit

i.e. weakness of one arm or one side of face

usually in the white matter beneath the cerebral cortex

due to disease of small vessels within the brain substance

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22
Q

posterioer ciruclaion stroke

A

stroke affecting structures supplied by the vertebro-basilar system

includes cerebellum, brainstem, cranial nuclei, occipital lob and long motor sensory tracts

effects include cranial nerve palsies, problems with movement coordination (cerebellar ataxia)

visual field loss from occipital lob damage and hemi paraesis due to nerve pathways from cortex to brainstem

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23
Q

stroke

think FAST

A

F ace - can pt smile, droop to one side?

A rms - can they raise both arms and grip you hand?

S peech - can they understand what you are saying and reply coherently and with articulated speech?

T ime - call 999

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24
Q

stroke aetiology

A

infaction 85%

  • embolic stroke - AF; Heart valve disease, recent MI
  • atheroma of cerebral vessels - carotid bifurcation, internal carotid, vertebral artery

haemorrhage 10% - aneurysm rupture

sub-arachnoid haemorrhage 5%

venus thrombosis <1%

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25
Q

stroke risk factors

A

hypertension - diastolic 110mmHg then 15x greater risk, even borderline hypertension has massively inc risk

smoking

alcohol

ischaemic heart disease

atrial fibrilation - atria never completely empty, clots form and are fired off from the aorta as emboli

diabetes mellitus

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26
Q

less common causes of stroke

A

venous thrombosis

  • OCP use
  • polycythaemia
  • thrombophilia - factor V Leiden

border zone infarction

  • severe hypotenion - hypoxic damage
  • cardiac arrest - if BLS carried out for more than 5 mins then permanent damage is usually seen

vasculitis

  • inflammation of vessek, sjorgen’s syndrome is a vasculitis disease so increase risk of stroke
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27
Q

stroke prevention

A

diet, smoking, alcohol, antiplatets

anticoagulants - apixiban

carotid endarterectomy - severe stenosis, previous TIA, <85 years old

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28
Q

investigations for stroke

A

Differentials - Infarct/Bleed/Subarachnoid Haemorrhage

Imaging

  • CT scan - rapid easy access but is poor for ischaemic stroke
  • MRI scan - difficult to obtain quickly, but better at visualising early changes of damage, MRA (Angiography) is best investigation for brain circulation
  • Digital subtraction angiography - if MRA isn’t available

*CT - brain bone space
*MRI - shows fluid and brain - better for stroke imaging > shows infarction unlike a CT

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29
Q

investigations for stroke risk factors

A

Carotid ultrasound

Cardiac ultrasound (LV thrombus)

ECG

Blood Pressure

Diabetes screen

Thrombophilia screen in young patients

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30
Q

effects of stroke

A

Loss of functional brain tissue

immediate nerve cell death

nerve cell ischaemia in penumbra (the area immediately outside an ischaemic area) > must be protected

Gradual or rapid loss of function

Some of the loss of function is due to inflammation - therefore time is the main teller in stroke recovery

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31
Q

complications of stroke

A

Motor function loss

  • Cranial nerve
  • Somatic nerves (opposite side) - can cause phantom limb sensation
  • Autonomic in brainstem lesions
  • Dysphonia
  • Dysphagia - can cause aspiration of food/saliva which can lead to pneuomnia and death because of the inability to choke/cough

Cognitive impairment

  • appreciation of things
  • Processing
  • understanding of speech/language
  • understanding of info
  • dysphasia/lexia/graphia/calculia

memory impairment

emotional lability and depression

32
Q

acute phase management of stroke

A

penumbra region - survivable ischamia - Nimodipin - Ca2+ blocker that has the added effect of reducing neurlogical deficit in delayed ischaemic strokes

improving perfusion - thrombolysis within 3 hrs - Alteplase - tissue plasminogen activator

maintain normoglycaemia - hypo/hyper harmful

remove haemoatoma - subarachnoid haemorrhage only

prevent future risk - Aspirin 300mg, anticoagulant if stroke caused by AF or LV thrombus, given 2 weeks after event

33
Q

chronic phase management of stroke

A

nursing and rehab

immobility support

  • bed sores - tissue necrosis from pressure on skin for too long
  • physiotherapy - prevent contracture

speech and language therapy

  • communications
  • swallowing and earing

occupational therapy

34
Q

dental relevance of stroke

A

Poor attendance and OH - due to mobility and dexterity issues

Communication difficulties - either due to muscles of speech or within brain

Risk of cardiac emergencies - MI or secondary stroke

Loss of protective reflexes

  • Aspiration
  • Managing saliva - Atropine (Anti-cholinergic) - antisialogogue

Loss of sensory infromation

difficulty in adapting to oral environment e.g new dentures

Stroke pain - CNS generated pain perception

35
Q

epilepsy associated with reduced levels of

A

GABA (gamma-Aminobutyric acid)

chief inhibitory neurotransmitter in the CNS

It reduces neuronal excitability throughout the nervous system

It is also directly responsible for regulation of muscle tone

In epilepsy levels of GABA are reduced in the brain - this leads to abnormal cell to cell message propogation

36
Q

classifications of epilepsy

A

generalised

  • tonic clonic
  • absence
  • myoclonic/atonic seizure

partial

  • simple
  • complex
  • simple sensory
37
Q

generalised tonic clonic seizure

A

a.k.a. grand mal seizures

loss of consiousness, muscle stiffness and convulsions and jerking for 1-3mins

tonic phase - stiffness, loss of consiousness and possibly noises

clonic phase - rapid and rhythmic jerking

start on one side of the brain and progress to the whole brain or sometimes just starts simultaneously on both sides

38
Q

absence seizures

A

Brief transient seizures where the person stops whatever activity they are doing for a brief time, and becomes
unresponsive but conscious, they may appear ‘absent’ or their eyes glaze over and drop what theyre holding

It usually only lasts half a minute maximum

aka petit mal seizure

may have mild tonic and clonic components but often almost inperceptible

Often associated with Porphyria in children as porphyrin inducing factors can cause these sizures

39
Q

myoclonic/atonic seizures

A

Happens to everyone at some point, i.e random foot jerk in bed, knee gives way when walking, hiccups etc

However with persistence it can be a sign of a neurological disorder

i.e CJD, Huntington’s Disease or Multiple Sclerosis

40
Q

simple partial seizures similar to

A

myoclonic seizures

41
Q

complex partial seizuress

A

can affect special senses, autonomic nervous system or GI organs

Jacksonian seizures localised to one particular area of brain

42
Q

simple sensry seizures

A

muslce jerking randomly in the face or limbs

43
Q

aetiology of epilepsy

A

idiopathic

trauma (head injury)

heatstroke - febrile seizure - hyperthermia remedied with anti-pyrexic drugs (paracetamol, ibuprofen)

CNS disease - tumour, stroke, CJD, meningitis, encephalitis

Social - late nights, alcohol, hypoglyceamia, flashing lights

44
Q

epilepsy preciptators

A

withdrawal/poor med compliance

epileptogenic drugs - some GA agents, alcohol, tricyclic antidepressants and selective serotonin, reuptake inhibitors

fatigue/stress, infection and menstruation

45
Q

prevenatative epilepsy tx

A

anticonvulsant drugs

  • valproate - increases GABA level at the GABA transaminase inhibitor
  • Carbamazepine - works well for myoclonic seizures
  • Phenytoin - Serotonin release agonist and also a SRI? action unsure
  • Gabapentin - reduces muscle spasticity and involuntary eye movement (nystagmus)
  • Phenobarbitone - Very cheap and effective anti-epileptic
  • Lamotrigine - Increases action of existing GABA, is chemically different than other anti-convulsants being a phenyltriazine
46
Q

emergency eplipetic tx

A

usually just supportive tx if unconcious - airway and O2

status epilepticus - use Benzodiazepines (e.g. Diazepam) GABA action inc at the GABAA receptor

47
Q

dental implications of epilepsy

A

Complications of fits

  • Oral soft tissue injury
  • dental injury/fracture

Complications of treatment

  • Gingival Hyperplasia (Phenytoin)
  • Bleeding tendency (Valproate)
  • Folate deficiency

Assess their risk of having a seizure

  • good and bad phases
  • ask when last three fits were
  • ask about medication compliance
  • ask about medication changes
48
Q

signs and symptoms of MS

A
  • muscle weakness
  • visual disturbance ] Optic neuritis
  • optic atrophy ] Optic neuritis
  • paraesthesia
  • autonomic dysfunction
  • dysarthria
49
Q

multiple sclerosis

A

Most common disorder of the CNS in the young

  • 8:1000 prevalence

CNS lesions only
Demyelination of axons
Usuallty patchy distribution
progressive functional loss over time

women in the 4th decade onet most severe

50
Q

aetiology of MS

A

Susceptibility acquired during childhood
altered host reaction vs infective agent
background in genetic immune factors
more common in identical twins
more common amongst immediate family members

generally unknown - combo genetic, environmental and social

51
Q

investigations for MS

A

MRI

CSF analysis - reduced lymphocytes, increased serum IgG level, visual evoked potentials (patterns on screense etc)

52
Q

prognosis of MS

A

Incurable and is degenerative
Steroids are good for acute exacerbations but cant cure

No effective treatment but just symptom management

  • Antibiotics
  • Antispasmodics - e.g Atropine for GI symptoms
  • Analgesics
  • PT and OT
53
Q

dental relevance of MS

A

limited mobility and psychological disorders

treat under LA

Orofacial motor and sensory disturbance in younger patients

Chronic Orofacial pain syndromes

Enhanced trigeminal neuralgia risk again in younger patients

54
Q

motor neuron disease

A

No sensory loss in this disease which helps to differentiate it from MS

Unknown aetiology but theorised to be viral in origin

Degeneration in the spinal cord (corticospinal tracts and anterior horns)

Bulbar motor nuclei i.e limbs etc

Patients aged 30-60 with a prognosis of 3 years of life after diagnosis

2.5:1 Male to female

55
Q

effects of motor neuron disease

A

progressive loss of motor function

  • limbs
  • intercostal
  • diaphragm
  • motor cranial nerves VII-XII

death due to

  • ventilation failure
  • aspiration pneumonia
56
Q

Tx for MND

A

None effective
PT and OT

Riluzole (delays MND by delaying the death of neurones to skeletal muscle) helps extend life 6-9 months

Aspiration prevention

  • PEG tube feed
  • Reduce salivation
57
Q

MND dental aspects

A

difficulty accepting care due to head an dneck weakness

realistic tx plannning

drooling and swallowing difficulties

58
Q

Parkinson’s disease

A

Degeneration of the dopaminergic neurons in the substantia nigra in the basal ganglia of the midbrain

50/50 male to female

cause unclear

  • may be due to previous Cerebrovascular disease or head trauma

drug induced - phenothiazine, butrophenones, valproate, metoclopramide

Associated parkinson’s dementia

59
Q

features of parkinson’s disease

A

bradykinesia

rigidity

tremor (slow amplitude)

postrual instability

60
Q

bradykinesia

A

slow movement and initiaion of said movement

61
Q

rigidity in parkinsons

A

inc muscle tone

62
Q

manifestations of parkinson’s

A

impaired gait and falls

impaired use of upper limbs

mask like face

swallowing problems

63
Q

Parkinson’s managament

A

treatment

medical - drugs can alleviate symptoms in early phase of disease

  • dopaminergic drugs
  • Levodopa with carbidopa - dopamine replacment
  • apomrphine - dopamine receptor anatgonist

PT and OT

sugical - sterotactic surgery, stem cell transplant

64
Q

dental aspiects of Parkinson’s

A

difficulty accepting tx

tremour at rest

facial tremor reduces purposeful movement e.g. chewing/mouth opening

dry moth from anticholinregic drugs

drug interactions

65
Q

myasthenia gravis

A

Antibody mediated autoimmune disease

Deficiency of function muscle ACh receptors that leads to muscle weakness

Disorder affects young women

Sometimes associated with Eaton-Lambert syndrome which is a disease of the NMJ in the hips and limbs

However in MG the muscles get weaker with activity but in straight ELS the muscles get stronger with activity

66
Q

Bell’s Palsy

A

Rapid onset
unilateral
ache behind the ear
Weakness worsens over 1-2 days

Prednisalone given for 5 days to reduce neural oedema

N.B, If bilateral presentation could be Sarcoidosis, Guillain-Barré syndrome or Melkersson-Rosenthal syndrome (Tongue fissures, unilateral facial palsy, facial swelling, similar lesions to crohn’s)

67
Q

ramsay-hunt syndrome Type 1

A

a.k.a Ramsay Hunt cerebellar syndrome

rare form of cerebellar degeneration which involves myoclonic epilepsy, progressive ataxia, tremor and dementing process

68
Q

Ramsay-hunt syndrome type 2

A

a.k.a Herpes Zoster Oticus

reactivation of varicella zoster in the geniculate ganglion of the brain (nerve bundle CNVII)

profound facial paralysis

vesicles in the pharynx

69
Q

cerebral palsy

A

disorder of the motor function secondary to cerbral damage

associated with birth injury/hypoxia

3 main types

  1. spastic - muscles contracted with associated epilepsy
  2. ataxic - cerebellar lesion results in disturbance of balance
  3. athetoid - writhing type movements
70
Q

spina bifida

A

vertebral arches fail to fuse

due to folate deficiency

may have inability to walk, epilepsy or learning difficulties or a combo of all three

71
Q

acoustic neuroma

A

benign tumour occuring at the cerbello pontine angle on the vestibular part of the vestibulocochlear nerve CNVIII

CNV, VII, IX and X may also be involved

leads to tinnitus, deafness and vertigo

facial twitching and parasthesias also possible, however these exclude the angle of the mandible which is innervated by the cervical nerves

72
Q

Huntington’s chorea

A

autosomal dominant disorder (chromosome 4)

progressive dementia (atrophy of the caudate nucleus of basal ganglia) with marked involuntary movements

doesn’t appear till middle age

Midazolam is a remarkable drug for people with this as a sedative

73
Q

Fridrich’s Ataxia

A

autosomal recessive disorder or sometimes sex linked degeneration of the spinal cord

can also lead to scoliosis, heart disease and diabetes

74
Q

6 types of dementia

A
  • *1) Alzheimer’s Disease** - Amyloid Beta and Tau protein
  • *2) Vascular dementia** - hypoxic degeneration
  • *3) Dementia with Lewy bodie**s - lewy bodies are abnormal protein aggregates that develop in neurons
  • *4) Parkinsons’s** - see notes above
  • *5) Frontotemporal Dementia** - personality changes
  • *6) Creutzfeld Jakob Disease** - caused by prions
75
Q

early, middle and late stage dementia features

A

Early stage - forgetfulness, losing track of time, lost in familiar places

Middle stage - forget names, lost at home, communication difficulty, need persona care, wandering, repeated questioning

Late stage - forget family, walking, recognising relatives and friends

76
Q

3 types of brain injury

A

traumatic brain injury

focal

diffuse

REVISION BDS (43 decks)

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