neurology p237 Flashcards

(76 cards)

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
stroke risk factors
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
26
less common causes of stroke
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
27
stroke prevention
diet, smoking, alcohol, antiplatets anticoagulants - apixiban carotid endarterectomy - severe stenosis, previous TIA, \<85 years old
28
investigations for stroke
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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investigations for stroke risk factors
Carotid ultrasound Cardiac ultrasound (LV thrombus) ECG Blood Pressure Diabetes screen Thrombophilia screen in young patients
30
effects of stroke
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
31
complications of stroke
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
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acute phase management of stroke
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
chronic phase management of stroke
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
dental relevance of stroke
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
epilepsy associated with reduced levels of
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
classifications of epilepsy
generalised * tonic clonic * absence * myoclonic/atonic seizure partial * simple * complex * simple sensory
37
generalised tonic clonic seizure
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
absence seizures
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
myoclonic/atonic seizures
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
simple partial seizures similar to
myoclonic seizures
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complex partial seizuress
can affect special senses, autonomic nervous system or GI organs Jacksonian seizures localised to one particular area of brain
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simple sensry seizures
muslce jerking randomly in the face or limbs
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aetiology of epilepsy
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
epilepsy preciptators
withdrawal/poor med compliance epileptogenic drugs - some GA agents, alcohol, tricyclic antidepressants and selective serotonin, reuptake inhibitors fatigue/stress, infection and menstruation
45
prevenatative epilepsy tx
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
emergency eplipetic tx
usually just supportive tx if unconcious - airway and O2 status epilepticus - use Benzodiazepines (e.g. Diazepam) GABA action inc at the GABAA receptor
47
dental implications of epilepsy
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
signs and symptoms of MS
- muscle weakness - visual disturbance ] Optic neuritis - optic atrophy ] Optic neuritis - paraesthesia - autonomic dysfunction - dysarthria
49
multiple sclerosis
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
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aetiology of MS
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
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investigations for MS
MRI CSF analysis - reduced lymphocytes, increased serum IgG level, visual evoked potentials (patterns on screense etc)
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prognosis of MS
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
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dental relevance of MS
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
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motor neuron disease
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
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effects of motor neuron disease
progressive loss of motor function * limbs * intercostal * diaphragm * motor cranial nerves VII-XII death due to * ventilation failure * aspiration pneumonia
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Tx for MND
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
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MND dental aspects
difficulty accepting care due to head an dneck weakness realistic tx plannning drooling and swallowing difficulties
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Parkinson's disease
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
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features of parkinson's disease
bradykinesia rigidity tremor (slow amplitude) postrual instability
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bradykinesia
slow movement and initiaion of said movement
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rigidity in parkinsons
inc muscle tone
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manifestations of parkinson's
impaired gait and falls impaired use of upper limbs mask like face swallowing problems
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Parkinson's managament
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
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dental aspiects of Parkinson's
difficulty accepting tx tremour at rest facial tremor reduces purposeful movement e.g. chewing/mouth opening dry moth from anticholinregic drugs drug interactions
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myasthenia gravis
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
Bell's Palsy
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)
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ramsay-hunt syndrome Type 1
a.k.a Ramsay Hunt cerebellar syndrome rare form of cerebellar degeneration which involves myoclonic epilepsy, progressive ataxia, tremor and dementing process
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Ramsay-hunt syndrome type 2
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
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cerebral palsy
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
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spina bifida
vertebral arches fail to fuse due to folate deficiency may have inability to walk, epilepsy or learning difficulties or a combo of all three
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acoustic neuroma
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
Huntington's chorea
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
Fridrich's Ataxia
autosomal recessive disorder or sometimes sex linked degeneration of the spinal cord can also lead to scoliosis, heart disease and diabetes
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6 types of dementia
* *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
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early, middle and late stage dementia features
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
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3 types of brain injury
traumatic brain injury focal diffuse