neurology p237 Flashcards
astrocytes
regulate transmission of signals in the brain
provide nutrients
create the blood brain barrier along with endothelial cells
microglia
act as housekeepers in the nervous system, dealing with waste and pathogens
antigen presentation
cytotoxicity
ependymal cells
line the ventricles of the brain and central canal of the spinal cord
produce CSF
role in neuroregeneration when damaged
Schwann cells
provide myelination to axons in PNS
oligodendrocytes
provide myelination to axons in CNS
Peripheral nervous system
types of sensory neurons 4
Aα - Myelinated, very large diameter
Aβ - Myelinated, large diameter
Aδ - Myelinated, small diameter
C - Unmyelinated, small diameter
peripheral nerve roles
carry information to and from the CNS
afferent (sensory) nerves
➡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
efferent (motor) nerves
➡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
central nervous system comprises
brain and spinal cord
brain
perceives and processes sensory stimuli
executes voluntray motor responses through skeletal muscle
regulates hoemostatic mechanisms (autonomic)
spinal cord
initiates reflexes from ventral horn and lateral horn grey matter
pathways for sensory and motor fucntions between periphery and brain
white matter
consists of axons and oligodendrocytes (the myelination of the latter gives its dark appearance)
grey matter
contains neurons and unmyelinated fibres
autonomic nervous system
hypothalamis controls ANS activity
subconcious cerbral input via limbic system
spinal cord too
stroke
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
Transiet ischaemic attack caused
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
types of stroke
total anterior circulation stroke
partial anterior ciculation stroke
lacunar stroke
posterior ciruclation stroke
total anteiror circulation stroke
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
partial anterior circulation stroke
not as severe as total
doesn’t have the higher cerebral function involvement
lacunar stroke
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
posterioer ciruclaion stroke
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
stroke
think FAST
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
stroke aetiology
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%
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
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
stroke prevention
diet, smoking, alcohol, antiplatets
anticoagulants - apixiban
carotid endarterectomy - severe stenosis, previous TIA, <85 years old
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
investigations for stroke risk factors
Carotid ultrasound
Cardiac ultrasound (LV thrombus)
ECG
Blood Pressure
Diabetes screen
Thrombophilia screen in young patients
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
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
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
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
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
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
classifications of epilepsy
generalised
- tonic clonic
- absence
- myoclonic/atonic seizure
partial
- simple
- complex
- simple sensory
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
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
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
simple partial seizures similar to
myoclonic seizures
complex partial seizuress
can affect special senses, autonomic nervous system or GI organs
Jacksonian seizures localised to one particular area of brain
simple sensry seizures
muslce jerking randomly in the face or limbs
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
epilepsy preciptators
withdrawal/poor med compliance
epileptogenic drugs - some GA agents, alcohol, tricyclic antidepressants and selective serotonin, reuptake inhibitors
fatigue/stress, infection and menstruation
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
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
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
signs and symptoms of MS
- muscle weakness
- visual disturbance ] Optic neuritis
- optic atrophy ] Optic neuritis
- paraesthesia
- autonomic dysfunction
- dysarthria
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
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
investigations for MS
MRI
CSF analysis - reduced lymphocytes, increased serum IgG level, visual evoked potentials (patterns on screense etc)
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
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
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
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
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
MND dental aspects
difficulty accepting care due to head an dneck weakness
realistic tx plannning
drooling and swallowing difficulties
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
features of parkinson’s disease
bradykinesia
rigidity
tremor (slow amplitude)
postrual instability
bradykinesia
slow movement and initiaion of said movement
rigidity in parkinsons
inc muscle tone
manifestations of parkinson’s
impaired gait and falls
impaired use of upper limbs
mask like face
swallowing problems
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
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
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
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)
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
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
cerebral palsy
disorder of the motor function secondary to cerbral damage
associated with birth injury/hypoxia
3 main types
- spastic - muscles contracted with associated epilepsy
- ataxic - cerebellar lesion results in disturbance of balance
- athetoid - writhing type movements
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
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
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
Fridrich’s Ataxia
autosomal recessive disorder or sometimes sex linked degeneration of the spinal cord
can also lead to scoliosis, heart disease and diabetes
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
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
3 types of brain injury
traumatic brain injury
focal
diffuse
