Neuro Flashcards
(48 cards)
Types of ascending tract and functions
Why is this clinically relevant?
The ascending tracts refer to the neural pathways by which sensory information from the peripheral nerves is transmitted to the cerebral cortex:
1) The Dorsal Column-Medial Lemniscal Pathway*
- first order neurones carry FINE touch, proprioception or vibration from the PNS to the medulla oblongata
- Signals from the upper limb (T6 and above) – travel in the fasciculus cuneatus (the lateral part of the dorsal column).
- Signals from the lower limb (T7 and below) travel via fasciculus gracilis (the medial part of the dorsal column). They then synapse in the nucleus gracilis and decussate at the medulla oblongata.
2) The Anterolateral System
- Anterior spinothalamic tract – carries the sensory modalities of crude touch and pressure.
- Lateral spinothalamic tract – carries the sensory modalities of pain and temperature.
After synapsing with the first order neurones, these fibres decussate within the spinal cord.
Clinical Relevance:
A lesion of the DCML pathway causes a loss of proprioception and fine touch. If the lesion occurs in the spinal cord (which is most common), the sensory loss will be ipsilateral – decussation occurs in the medulla oblongata. DCML lesions can be seen in vitamin B12 deficiency and tabes dorsalis (a complication of syphilis).
Injury to the anterolateral system will produce an impairment of pain and temperature sensation. In contrast to DCML lesions, this sensory loss will be contralateral (the spinothalamic tracts decussate within the spinal cord).
Brown-Sequard syndrome
Brown-Séquard syndrome refers to a hemisection (one sided lesion) of the spinal cord. This is most often due to traumatic injury, and involves both the anterolateral system and the DCML pathway:
DCML pathway – ipsilateral loss of touch, vibration and proprioception.
Anterolateral system – contralateral loss of pain and temperature sensation.
It will also involve the descending motor tracts, causing an ipsilateral hemiparesis.
Types of motor tracts
Pyramidal and Extrapyramidal
Pyramidal tracts – These tracts originate in the cerebral cortex, carrying motor fibres to the spinal cord and brain stem. They are responsible for the voluntary control of the musculature of the body and face.
These pathways are responsible for the voluntary control of the musculature of the body and face.
1) Corticospinal tracts – supplies the body. pyramidal decussation in ventral medulla
2) Corticobulbar tracts – supplies the head and neck.
Extrapyramidal tracts – These tracts originate in the brain stem, carrying motor fibres to the spinal cord. They are responsible for the involuntary and automatic control of all musculature, such as muscle tone, balance, posture and locomotion
There are no synapses within the descending pathways. At the termination of the descending tracts, the neurones synapse with a lower motor neurone. Thus, all the neurones within the descending motor system are classed as upper motor neurones.
Cerebellar symptoms and common causes
Symptoms • Dysdiadokinesia • Dysmetria: past-pointing • Ataxia: limb / trunkal • Nystagmus: horizontal = ipsilateral hemisphere • Intention tremor • Speech: slurred, staccato, scanning dysarthria • Hypotonia Causes: PASTRIES Malginancy e.g. Paraneoplastic (eg bronchial Ca); CPA Alcohol: thiamine and B12 deficiency • M Sclerosis • Tumor: e.g. CPA lesion • Rare: MSA, Friedrich’s, Ataxia Telangiectasia Iatrogenic: phenytoin Endocrine: hypothyroidism Vascular such as Stroke: vertebrobasilar
Dementia definition
types + path
management
Definition: Chronically impaired cognition that affects multiple domains: memory, attention, language; No impairment of consciousness; Acquired and progressive
1) Alzheimers- neurofibrillary tangles and β amyloid plaques; cholinesterase inhibitors (donepezil, rivastigmine) if MMSE is 10-20
2) Vascular dementia - sudden onset, stepwise deterioration, patchy deficits, vascular RFs, management is treatment of underlying cause
3) Lewy Body dementia - Lewy Bodies in occipito-parital cortex; PC: Fluctuating cognitive dysfunction, visual hallucinations, parkinsonism; Rx: cholinesterase inhibitors
4) Frontotermporal Dementai - Pick’s disease due to Pick Bodies; PC: disinhibition, personality change, early memory preservation, progressive aphasia; Ix: MRI – frontal or temporal atrophy
Delirium causes
• Drugs: opioids, sedatives, L-DOPA • Eyes, ears and other sensory deficits • Low O2 states: MI, stroke, PE • Infection • Retention: stool or urine • Ictal • Under- hydration / -nutrition • Metabolic: DM, post-op, sodium, uraemia • Subdural haemorrhage or other intracranial pathology Mx: • ID and Rx underlying cause • Surround ¯c familiar people • Nurse in moderately lit, quiet room • Find glasses, hearing aids… • Avoid sedatives if possible, but if disruptive
Management of the different causes of headache
- Meningitis -Communnity Ben Pen 1.2g IM; In hospital: IV Cef + Amox >60, Dex, fluids. Do LP if they aren’t shock/CI
- Migraine - Rescue: NSAID, sumatriptan (inpt: IV antiemetic + diphenhydramine). Preventative: propanolol, TCA at lower dose, anticonvulsant topiramate, valproate
- Cluster - O2 via non-rebreathe mask, Sumitriptan, Prevention: verapamil, topiramate, Li
- Hemicrania - indomethacin
- Trigeminal Neuralgia: exclude 2O cause by MRI; Med: carbamazepine, lamotrigine, gabapentin; Rx Surg: microvascular decompression or radiosurgery (focussed radiation)
- Analgesia overuse: Use OTC analgesia on 6 days/month max
- GCA rule of 60 (60 year old ESR over 60 and 60mg pred) (Unilateral temple/scalp pain and tenderness. Thickened, pulseless temporal artery. Jaw claudication, amaurosis fugax, sudden blindness. Assoc:PMR in 50%; ESR↑↑↑, plats↑, ALP↑, Hb↓, temporal artery biopsy
Mx; High dose pred (60mg/d PO) for 5-7d Guided by symptoms and ESR. Give PPI+bisphosphonate. Prog: 2yr course then complete remission
SAH Ix and Mx
CT: Detects >90% of SAH w/i first 48hrs
LP: If CT-ve and no CIs >12h after start of headache; Xanthochromia due to breakdown of bilirubin
MRI - important for location of bleed which would could help with the cause and long term mx. (Subcortical = HTN bleeds, eventually AC; Microbleeds/Cortical bleeds - Amyloid and therefore no AC; Tumour- wouldn’t AC)
Mx
This is an acute emergency and therefore I would carry out in A-E, escalate to a senior immediately.
C: Supportive care and Frequent neuro observation: pupils every 20 min, GCS, BP, stop any ongoing anticoagulants, place an arterial line
Maintain CPP: keep SBP >160
M: Nimodipine for 3wks ↓ cerebral vasospasm, if seizures occur if na valp
S: Endovascular coiling (preferable to surgical clipping)
Stroke non- acute management
Secondary Prevention:
C: Optimise cardiovascular risk factor control + MENDS
I would use the modified rankin scale to assess extent of disability immediately post stroke and then throughout rehab.
M:
Aspirin / clopi 300mg for 2wks after stroke then either
- Clopidogrel 75mg OD (preferred option) or
- Aspirin 75mg OD + dipyridamole MR 200mg BD or
- Warfarin instead of aspirin/clopidogrel if
• Cardioembolic stroke or chronic AF
• Start from 2wks post-stroke (INR 2-3)
• Don’t use aspirin and warfarin together.
- If they were HTN, diagnose and start antihypertensives
- Start high intensity statin (such as atorvastatin 20–80mg daily) after TIA/stroke diagnosis, no sooner than 48 hours
- If AF caused the stroke, asses anticoag with chadvasc,
S: Carotid endarterectomy if medically fit and symptomatic stenosis ≥70%
Rehab: MENDS
MDT: physio, SALT, dietician, OT, specialist nurses, neurologist, family
Eating- Screen swallowing: refer to specialist; NG/PEG if unable to take oral nutrition; Screen for malnutrition (MUST tool)
Neurorehab: physio and speech therapy
DVT Prophylaxis
Sores: must be avoided @ all costs
Stroke acute management
To suspect a stroke I would use the FAST /ROSIER tool (Rosier likeliness of stroke 5 crriteria)
This is a medical emergency so I would do an A-E, DEFG! (keep glucose 4-11) and escalate to my senior immediately.
CT to rule out Haemorrhage
Aspirin 300mg and thrombolysis <4.5 hours
- Can give thrombectomy <6 hours (up to 24 hrs) if CTA /MRA shows confirmed occlusion of PAC.
I can use the NIH Stroke Scale to assess the severity of stroke, and that can be used to guide decision for thrombectomy i.e. 6 and above -> consider thrombectomy.
Furthermore, the MRS can be used to quantify the extent of disability to assess whether thrombectomy is appropriate usual cut off is 2 or below.
The bamford stroke classification can also be used in the absence of imaging to identify the likely location of the stroke.
Use the BAMFORD stroke classification
- Unilateral sensory/weakness of face, arm and leg
- Homonymous hemianopia
- Higher cerebral dysfunction (dysphasia, visuspatial disorder)
3/3 = total anterior circulation stroke; 2/3 = partial ACS
- POCS -> if posterior circulation signs i.e. cerebellar or brainstem
- LACS -> lacunar
TIA management
FAST /ROSIER tool
A-E, DEFG!
300mg Aspirin unless CI
- Dont CT routinely unless you want to rule out other ddx
- Refer to TIA specialist clinic within 24 hrs (don’t use ABCD2), after consider MRI
- After TIA diagnosis confirmed, offer 2ndary prevention
- Use DUSS, CTA and MRA to elicit % of stenosis if >50% consider endarcetomy
ACAS
A- antiplatelet - Aspirin/clopi 300mg/d for 2wks then 75mg/d
C- Cardio risk factor management (BP, statin, lipids, DM)
A - ABCD2 score to predict subsequent stroke
S- Specialist referral to TIA clinic
SDH and EDH management
SDH - 1st line: irrigation/evacuation via burr-hole craniostomy; 2nd line: craniotomy; Address causes of trauma
EDH
• Neuroprotective ventilation (O2>100, CO2 35-40)
• Consider mannitol (1g/kg IV via central line)
• Craniectomy for clot evacuation and vessel ligation
Encephalitis PC and Mx
PC: • Infectious prodrome: fever, rash, LNs, cold sores, conjunctivitis, meningeal signs. • Bizarre behaviour or personality change • Confusion • ↓ GCS → coma • Fever • Headache • Focal neuro • Seizures • Hx of travel or animal bite
mx:
Aciclovir STAT: 10mg/kg/8h IVI over 1h for 14/7
Supportive measures in HDU/ITU
Phenytoin for seizures
Head injury CT indications
Break: open, depressed or base of skull Amnesia >30min retrograde Neuro deficit or seizure GCS: <13 @ any time or <15 2h after injury Sickness: vomited > once LOC or any amnesia and any of: • Dangerous mechanism: RTA, great height • Age ≥ 65 • Coagulopathy (inc. warfarin) BANGS LOC
Secondary survey for head injury
Look for: • Lacerations • Obvious facial/skull deformity • CSF leak from nose or ears • Battle’s sign, Racoon eyes • Blood behind TM • C-spine tenderness ± deformity Head-to-toe examination for other injuries Log role
When do you admit head injury and how do you manage them
Neurosurgical opinion if signs of ↑ICP, CT evidence of intracranial bleed significant skull # Admit if: • Abnormalities on imaging • Difficult to assess: EtOH, post-ictal • Not returned to GCS 15 after imaging • CNS signs: vomiting, severe headache Neuro-obs half-hrly until GCS 15 • GCS • Pupils • HR, BP • RR, SpO2 • Temperature
Discharge advice for head injury
- Stay with someone for first 48hrs
- Give advice card advising return on:
- Confusion, drowsiness, unconsciousness
- Visual problems
- Weakness
- Deafness
- V. painful headache that won’t go away
- Vomiting
- Fits
Head injury seizure management
- Treat seizures
- Lorazepam 2-4mg IV
- Phenytoin18mg/kg IVI then 100mg/6-8h
Parkinsonism Ddx
- Idiopathic - Parkinson’s DIsease
- Parkinson’s plus syndromes (basal ganglia degeneration as well as other systems)
- Multiple system Atrophy
- Progressive supranuclear palsy
- Corticobasal degeneration
- Lewy Body Dementia - Drugs e.g. metoclopromide, chlorpromazine, 1st gen antipsychotics
- Wilsons Disease
- Trauma: Dementia Pugilistica (repeated brain trauma -> chronic traumatic encephalopathy)
- Infection: syphillis, HIV CJD
All the features of parkinsons disease
• Asymmetric onset: side of onset remains worst
TRAPPS PD
• Tremor: ↑ by stress, ↓ by sleep
• Rigidity: lead-pipe, cog-wheel
• Akinesia: slow initiation, difficulty ¯c repetitive movement, micrographia, monotonous voice, mask-like face
• Postural instability: stooped gait ¯c festination
• Postural hypotension: + other autonomic dysfunction*
• Sleep disorders: insomnia, EDS, OSA, RBD
• Psychosis: esp. visual hallucinations
• Depression / Dementia / Drug SEs
*Constipation, hypersalivation, urgency
Management of PD
DAT-SCAN - single-photon emission computed tomography (SPECT) imaging technique that helps visualize dopamine transporter levels in the brain CMS: C: MDT approach, PT, OT, nurse specilalist, assess disability using UPDRS*, depression screening M: Young onset + biologically fit: 1 Da agonists: ropinirole, pramipexole 2 MAO-B I rasagiline, selegiline 3 LDOPA co-careldopa or co-beneldopa
Biologically frail + comorbid
1 LDOPA 2 MAO-B I
S: Deep brain stimulation & interrupt basal ganglia
*UPDRS: Unified Parkinson’s Disease Rating Scale for disability assessment
Other adjunct therapies in PD
COMT inhibitor: tolcapone, entacapone − Lessen end-of-dose effect Apomorphine: potent Da agonist − SC rescue pen for sudden “off” freezing Amantidine: weak Da agonist − Rx of drug-induced dyskinesias Atypical antipsychotics: e.g. quetiapine − Disease-induced psychosis SSRIs: citalopram, sertraline − Depression
What is MS?
A chronic inflammatory condition of the CNS characterised by multiple plaques of demyelination disseminated in time and space.
Path: CD4 cell-mediated destruction of oligodendrocytes → demyelination and eventual neuronal death.
MS Presentation
Presentation: Tingling Eye: optic neuritis (↓ central vision + eye move pain) Ataxia + other cerebellar signs Motor: usually spastic paraparesis
Features:
Cerebellar: falls, scanning dysarthria, trunk and limb ataxia,
Eye: Diplopia, optic neuritis, bilateral INO
Motor: Spastic weakness, transverse myelitis
Sensory: Dys/paraesthesia, decreased vibration and trigeminal neuralgia
GI: Swallowing disorders, Constipation
Sexual/GU: ED + anorgasmia, Retention, Incontinence
Signs:
Lhermitte’s sign - Neck flexion → electric shocks in trunk/limbs
Uhtoffs phenomenon - Raised body temperature resulting in exacerbation of symptoms
