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.
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-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
types + path
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
• 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)
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
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.
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%
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
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
FAST /ROSIER tool
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
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
• 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
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
- V. painful headache that won’t go away
Head injury seizure management
- Treat seizures
- Lorazepam 2-4mg IV
- Phenytoin18mg/kg IVI then 100mg/6-8h
- 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
• 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.
Presentation: Tingling Eye: optic neuritis (↓ central vision + eye move pain) Ataxia + other cerebellar signs Motor: usually spastic paraparesis
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
Lhermitte’s sign - Neck flexion → electric shocks in trunk/limbs
Uhtoffs phenomenon - Raised body temperature resulting in exacerbation of symptoms
Transverse myelitis is a rare autoimmune neurological disorder caused by inflammation across both sides of one level or segment of the spinal cord
Prognosis: Reversible but can take months - years
MRI diagnosis and Ix
Diagnosis: Demonstration of lesions disseminated in time and space, can use McDonald Criteria (criteria if the clinical evidence isn’t clear for 2 lesion)
MRI: Gd-enhancing or T2 hyper-intense plaques
- Gd-enhancing = active inflammation
- Typically located in periventricular white matter
LP: Lymphocytosis and IgG oligoclonal bands (not present in serum, not specific)
- Anti-MBP (increases per relapse)
- NMO-IgG: highly specific for a ddx Devic’s syn.
Evoked potentials: delayed auditory, visual and sensory
1) MDT: neurologist, radiologist, physio, OT, specialist nurses, GP, family
2) Acute Attack:
Methylpred 1g IV/PO /24h for 3d (decreased duration and severity of attack, does not affect long term)
- Biologicals: IFN-β: ↓ relapses by 30% in relapsing remitting MS
- DMARDs: Natalizumab in RRMS, 2nd line Alemtuzumab
4) Symptomatic relief
• Fatigue: modafinil
• Depression: SSRI (citalopram)
• Pain: amitryptylline, gabapentin
• Spasticity: physio, baclofen,
• Urgency / frequency: oxybutynin, tolterodine
• ED: sildenafil
• Tremor: clonazepam
Types of MS
Classification: • Relapsing-remitting: 80% • Secondary progressive • Primary progressive: 10% • Progressive relapsing
- Disruption of MLF connecting CN6 to CN3
- Weak adduction of ipsilateral eye
- Nystagmus of contralateral eye
- Convergence preserved
- PC: pain on eye movement, rapid ↓ central vision
- Uhthoff’s: vision ↓ ¯c heat: hot bath, hot meal, exercise
- o/e: ↓ acuity, ↓ colour vision, white disc, central scotoma, RAPD
Poor prognostic indicators in MS
- Motor signs @ onset (sensory = good prog)
- Many relapses early on (shorter interval between them)
- Many MRI lesions and axonal loss
S1 root conversion
- Weak foot plantarflexion and eversion
- Loss of ankle-jerk
- Calf pain
- Decreased sensation over sole of foot and back of calf
Foot drop differential
Think anterior horn cell—nerve root—plexus—peripheral nerve—NMJ—muscle
Muscle (weak anterior tibialis): any cause of myopathy
Nerve (common peroneal nerve palsy): mono/polyneuropathy eg. trauma to fibular head, surgery on leg, compression of fibula neck by cast/tourniquet/leg crossing/bandaging, mononeuritis multiplex of any cause
Sciatic nerve palsy eg. trauma, IM injection
Lumbosacral plexopathy eg. trauma, tumour
L5 root lesion eg. prolapsed disc
Anterior horn cell eg. motor neuron disease (NB: no sensory deficit)
Spinal cord or brain lesion (stroke, space-occupying lesion, demyelination)- causing bilateral foot drop
Bulbar vs Pseudobulbar palsy
- Diseases of nuclei of CN 9-12 in the medulla
- LMN lesions of tongue, talking and swallowing
Flaccid, fasciculating tongue
Speech: quiet or nasal (“Donald Duck” speech)
Normal / absent jaw jerk
Loss of gag reflex
Causes: MND, GBS, MG, Central pontine myelinolysis (CPM)
Pseudobulbar / Corticobulbar Palsy
- Commoner than bulbar palsy
- Bilateral lesions above mid-pons (e.g. corticobulbar
tracts) → UMN lesions of swallowing and talking
- CN motor nuclei have bilateral cortical
representation except lower half of CN7
Slow tongue movements c¯ slow deliberate
speech: “hot-potato” speech
Brisk jaw jerk
Causes: MS, MND, Stroke
MND sub types
- Amyotrophic lateral sclerosis (50%): Mixed upper and lower motor neurone signs
- Primary lateral sclerosis: Upper motor neurone signs only
- Progressive muscular atrophy: Lower motor neurone signs only
- Progressive bulbar/pseudobulbar palsy – affects CN 9-12
3rd palsy presents how? causes?
Ptosis: Due to paralysis of LPS (levator palpebrae superioris) muscle
Ocular deviation: In case of third-nerve palsy, the lateral rectus and superior oblique are spared, and their unopposed action brings the eye in a “down and out” position.
Pupil: In compressive third-nerve palsy, the pupil becomes fixed and dilated due to paralysis of sphincter pupillae - Myhydriasis. Ciliary muscle paralysis also leads to loss of accommodation. However, in ischaemic lesions, the pupil is spared, and there is no loss of accommodation (partial).
Diplopia: This occurs due deviation of the affected eye resulting in the image falling on an extrafoveal point. However, due to ptosis the patient usually doesn’t complain of double vision as ptosis acts as a barrier to diplopia.
Causes: Vascular ischemia (HTN most common)
Trauma, Intracranial neoplasm, Hemorrhage
Which CN does which eye muscles?
LR6(SO4)3 is a simple mnemonic representing the innervation of the extraocular muscles. It stands for:
LR6: Lateral rectus muscle which is supplied by the sixth cranial nerve
SO4: Superior oblique muscle which is supplied by the fourth cranial nerve
3: The third cranial nerve supplies other extraocular muscles
CN III syndromes
Benedikt syndrome: Ipsilateral third-nerve palsy and contralateral tremors
Weber syndrome: Ipsilateral third-nerve palsy and contralateral hemiplegia
Nothnagel syndrome: Ipsilateral third-nerve palsy and cerebellar ataxia
Claude syndrome: Combined features of both Benedikt and Nothnagel syndromes
CN III management
C- short term measure. Most patients with ischemic third-nerve palsy demonstrate improvement within 1 month and complete recovery in 3 months
S- In pupil-sparing cases, surgical treatment is advised after 6 months in acquired palsies, if there is no improvement in symptoms.
Secondary to injury of the sympathetic nervous pathways resulting loss of vasomotor tone and failure of the heart to increase causing profound Hypothension that may be mistake for hypovolaemia
Hypotension + Bradycardia + warm extremitis
Mx: ionotropes (NA, vasopressin), Atropine to reverse brady
Causes: Spinal cord injury above T5
Spinal shock - occurs after acute sc transection and involves loss of all voluntary and reflex activity below injury level (hypertonic paralysis, loss of sensation and bladder retention)
A posterior circulation syndrome (POCS) involves damage to the area of the brain supplied by the posterior circulation (e.g. cerebellum and brainstem).
One of the following need to be present for a diagnosis of a POCS:
Cranial nerve palsy and a contralateral motor/sensory deficit
Bilateral motor/sensory deficit
Conjugate eye movement disorder (e.g. horizontal gaze palsy)
Cerebellar dysfunction (e.g. vertigo, nystagmus, ataxia)
Isolated homonymous hemianopia
Decompesnated myasthenia Gravis
IVIG and PEX
A 69-year-old lady is brought to hospital by an ambulance crew with a suspected stroke. On review in the emergency department she is unable to speak although she is able to follow instructions which have been written down. She has no past medical history.
A blockage of which of the following cerebral arteries is most likely to be the cause of this woman’s symptoms?
The symptoms described here would fit with a form of aphasia (most likely global given her need for written instructions) and therefore her dominant hemisphere must be affected. Although you do not know the handedness of the patient in the scenario, the most likely affected side is the left as the percentage of right and left handed individuals with a dominant left hemisphere is 90% and 60% respectively, making the left always the most likely affected side regardless of handedness. The middle cerebral artery on the dominant side supplies both Wernicke’s and Broca’s areas of the cortex which are responsible for understanding and production of speech.
What are the features spared in MND?
No sensory signs
doesn’t affect external ocular muscles
no cerebellar signs
abdominal reflexes are usually preserved and sphincter dysfunction if present is a late feature
Nerve conduction studies in Guillain-Barre syndrome shows decreased motor nerve conduction velocity.
rise in protein with a normal white blood cell count (albuminocytologic dissociation) - found in 66%
Anterior cerebral artery infarct
Contralateral hemiparesis and sensory loss, lower extremity > upper
Posterior cerebral artery infarct
Contralateral homonymous hemianopia with macular sparing
Contralateral hemiparesis and sensory loss, upper extremity > lower
Contralateral homonymous hemianopia