Stroke, TIA
Stroke syndromes
strokesyndromes.pdf
https://pubs.rsna.org/doi/full/10.1148/rg.2019180126
CUH TIA referral form
Brainstem syndromes
| paresis | sensory | Coordination | Cranial Nerves | |
|---|---|---|---|---|
| Weber Syndrome paramedian branches of the basilar artery or posterior cerebral artery | Contralat hemi | Occ.contralateral parkinsonian rigidity. (if substantia nigra involveed) | Ipsilat CNIII: inferolateral eye deviation, diplopia, ptosis, afferent pupillary defect | |
| Benedikt Syndrome (paramedian midbrain syndrome) occlusion of branches of the posterior cerebral artery | crossed hemiataxia, and choreoathetosis | ipsilateral CNIII palsy | ||
| Claude Syndrome Occlusion of the small perforating branches of the posterior cerebral artery | contralateral upper and lower limb ataxia | ipsilateral CNIII palsy | ||
| Parinaud Syndrome (dorsal midbrain syndrome) usually space occ lesion near pineal | Triad: 1. upward gaze palsy 2. pupillary light-near dissociation (the pupil is poorly reactive to light but constricts with convergence) 3. convergence-retraction nystagmus |
|||
| Nothnagel Syndrome Mass or infarct of the superior cerebellar peduncle | ipsilateral cerebellar ataxia | unilateral or bilateral CNIII paralysis | ||
| Marie-Foix Syndrome (lateral pontine syndrome) | ||||
| Wallenberg syndrome (lat medullary syndrome) | Contralateral body pain/numbness | Ipsilateral facial pain/numbness Gait ataxia Dysphagia – difficulty swallowing Dysarthria – slurred speech Dysphonia – disorderly voice Palatal myoclonus – twitching mouth |
Lateral Medullary Syndrome (Wallenberg Syndrome)
- On the side of the lesion:
- Facial sensory loss
- Nystagmus
- Horner's syndrome
- Loss of gag reflex
- Ipsilateral ataxia with a tendency to fall to the ipsilateral side
- On the contralateral side:
- Pain and temperature sensory loss in the extremities
- Generally:
- Vertigo
- Nausea
- Dysphagia
NIH Stroke scale (NIHSS):
| Category | Description | Score | |
|---|---|---|---|
| 1a | level of consciousness (LOC) | Alert Drowsy Stuporous Coma | 0 1 2 3 |
| 1b | LOC questions (month, age) | Answers both correctly Answers 1 correctly Incorrect on both | 0 1 2 |
| 1c | LOC commands (open and close eyes grip and release nonparetic hand) | Obeys both correctly Obeys 1 correctly Incorrect on both | 0 1 2 |
| 2 | Best gaze (follow finger) | Normal Partial gaze palsy Forced deviation | 0 1 2 |
| 3 | Best visual (visual fields) | No visual loss Partial hemianopia Complete hemianopia Bilateral hemianopia | 0 1 2 3 |
| 4 | Facial palsy (show teeth, raise brows,squeeze eyes shut) | Normal Minor Partial Complete | 0 1 2 3 |
| 5 | Motor arm left* (raise 90°, hold 10 seconds) (preferably with the palm facing up) | No drift Drift Cannot resist gravity No effort against gravity No movement | 0 1 2 3 4 |
| 6 | Motor arm right* (raise 90°, hold 10 seconds) (preferably with the palm facing up) | No drift Drift Cannot resist gravity No effort against gravity No movement | 0 1 2 3 4 |
| 7 | Motor leg left* (raise 30°, hold 5 seconds) | No drift Drift Cannot resist gravity No effort against gravity No movement | 0 1 2 3 4 |
| 8 | Motor leg right* (raise 30°, hold 5 seconds) | No drift Drift Cannot resist gravity No effort against gravity No movement | 0 1 2 3 4 |
| 9 | Limb ataxia (finger-nose, heel-shin) | Absent Present in 1 limb Present in 2 limbs | 0 1 2 |
| 10 | Sensory (pinprick to face, arm, leg) | Normal Partial loss Severe loss | 0 1 2 |
| 11 | Extinction/neglect (double simultaneous testing) | No neglect Partial neglect Complete neglect | 0 1 2 |
| 12 | Dysarthria (speech clarity to “mama, baseball, huckleberry, tip-top, fifty-fifty”) | Normal articulation Mild to moderate dysarthria Near to unintelligible or worse | 0 1 2 |
| 13 | Best language (name items, describe pictures) | No aphasia Mild to moderate aphasia Severe aphasia Mute | 0 1 2 3 |
| Total | 0-42 |
Cerebellar stroke
- probably <2% of all strokes but much higher mortality rate
- secondary oedema can have more catastrophic consequences compared with supratentorial strokes
- ~75% report “dizziness” of some form, with a sensation of vertigo or falling to one side.
- inability to walk or only with difficulty, either due to ataxia or to focal or systemic “weakness.”
- >50% report nausea or vomiting
- symptoms often more severe than examination findings
- broad spectrum of presentations and can therefore may be misdiagnosed:
- vestibular neuronitis, migraine, syncope
- hypertensive emergency, renal failure, hypoglycaemia
- alcohol or drug intoxication
- MRI often required as bone density in lower skull reduces CT accuracy in diagnosing post fossa pathology
| artery | territory | signs and symptoms |  |
|---|---|---|---|
| sup CBLLR (SCA) | superior CBLLM post-lateral midbrain | ataxia, dysarthria, nystagmus N&V, headache, vertigo |
|
| ant inf CBLLR (AICA) | ant-inferior CBLLM post-lateral pons, inner ear | dysmetria, vertigo, N&V, head movement intolerance, Horner's, unilat deafness ipsilateral facial paralysis/anaesthesia, contralat pain & temp loss, ataxia |
|
| post inf CBLLR (PICA) | post-inferior CBLLM | headache, horizontal ipsilat nystagmus, truncal ataxia |
Vertebral artery dissection
- often young patient with severe occipital headache and neck pain
- often following head or neck injury which may seem trivial. eg neck manipulation or injury, Marfan syndrome, Ehlers Danlos syndrome, and fibromuscular dysplasia.
- often no weakness so often missed
- ataxia with falling to ipsilateral side is common
- focal CNS symptoms often delayed and usually attributed to lateral medullary effects (Wallenberg syndrome or post inf CBLLR art syndrome):
- Ipsilateral facial dysesthesia
- Ipsilateral loss of taste (nucleus and tractus solitarius)
- Dysarthria or hoarseness, Dysphagia (CN's IX & X)
- Contralateral loss of pain and temperature sensation in the trunk and limbs
- minimal or no contralateral weakness
- Hiccups, Vertigo
- Nausea and vomiting
- Diplopia or oscillopsia (image movement experienced with head motion)
- Disequilibrium
- Unilateral hearing loss
*if involvement beyond medulla, other signs of CLLR dysfunction occur and sometimes medial medullary syndrome
Carotid artery dissection
- be suspicious with unusual focal neurologic complaints especially if CN's involved
- headache before CNS symptoms vs following or accompanying with cerebral ischaemic strokes
- any patient who has sustained major trauma or even minor mechanism stress or direct impact on the neck
- associations include: chiropractic manipulation, yoga, gymnastics, sports injuries (especially with impact to the head & neck), overhead painting, coughing, or sneezing
- Headache, including neck and facial pain
- Transient episodic blindness (amaurosis fugax)
- Ptosis with miosis (partial Horner syndrome) – usually painful when caused by internal carotid artery dissections
- Neck swelling
- Pulsatile tinnitus ≤25% of patients
- Decreased taste sensation (hypogeusia)
- Focal weakness
- Migraine-like symptoms (eg, a scintillating scotoma)
Cerebral Amyloid Angiopathy
https://www.ncbi.nlm.nih.gov/books/NBK556105/
https://jnnp.bmj.com/content/88/11/982
- accumulation of amyloid beta-peptide within the leptomeninges and small/medium-sized cerebral blood vessels resulting in fragile vessels which lead to intracerebral hemorrhages.
- present as cognitive impairment, incidental microbleeds, hemosiderosis, inflammatory leukoencephalopathy, Alzheimer disease, or transient neurological symptoms
- familial and sporadic
- definitive Dx only on post-mortem exam but otherwise primarily by a combination of findings classified by Boston criteria
- definitive - post-mortem
- probable (with imaging) - Multiple haemorrhages restricted to the cortical, lobar, or cortical-subcortical regions or single lobar, cortical, or cortical-subcortical haemorrhage and focal or disseminated superficial siderosis, absence of another diagnostic lesion, age ≥55 years
- probable (with pathology) - Lobar, cortical-subcortical haemorrhage, or cortical haemorrhage, tissue evidence of CAA, absence of another diagnostic lesion
- possible (with imaging) - Single haemorrhage restricted to the cortical, lobar, or cortical-subcortical region or diffuse, superficial siderosis, absence of another diagnostic lesion, age ≥55 years
- recurrent ICH is common - therefore anti-platelet and anti-coagulation med's usually avoided
- Small trials have shown pulsed cyclophosphamide or glucocorticoids resulted in sustained clinical improvement.
- aside from diligent BP management to reduce risk of further bleeds, strategy of anti-convulsant therapy commonly employed in Mx of likely micro-bleeds
Croydon pathway
Imaging Protocol for Suspected Stroke and TIA
The London model has been set up since 2010. This means that all patients who are FAST positive (ie have face or arm weakness, or speech disturbance) should be brought initially to the 8 hyper-acute units.
However, there are some patients who still present to local hospitals either because the strokes are not FAST positive (posterior circulation strokes) or are too unwell to be transferred to a HASU. There are also some patients who self-present to local A&Es with suspected strokes.
PATIENTS PRESENTING AS ACUTE STROKES
- If symptoms are < 3 hours
- Patients should have urgent blue-light transfer to nearest available HASU.
- If symptoms > 3hours but <24 hours, patients should be ideally be transferred to HASU - St George's Stroke Reg. Option 2, Bleep 7317
- However, due to capacity issues, they may decline to take patients and request that patients be treated locally.
Imaging for patients presenting as acute strokes Brain imaging should be performed immediately[16] for people with acute stroke if any of the following apply:
- early anticoagulation treatment
- on anticoagulant treatment
- a known bleeding tendency
- a depressed level of consciousness (Glasgow Coma Score below 13)
- unexplained progressive or fluctuating symptoms
- papilloedema, neck stiffness or fever
- severe headache at onset of stroke symptoms.
For all people with acute stroke without indications for immediate brain imaging, scanning should be performed as soon as possible
Patients presenting with TIAs
In patients who have a suspected TIA ( ie – signs and symptoms have completely resolved within 24 hours) should be assessed and have an ABCD2 score done.
- High risk TIA patients
- Patients who have ABCD2 score ≥4 or have had > 1 episode are classed as high risk TIAs and have to have assessment by a specialist within 24 hours of presenting to an initial health care professional.
Patients who present on Sunday to Thursday and during the day on Friday, should be referred directly to the open access TIA clinic and have the appropriate investigations arranged by the clinicians in the clinic.
This would include brain imaging – either CT or MRI and Carotid dopplers.
Weekend imaging Patients presenting late on Friday and Saturday with ABCD2 score ≥4 or more or have had more than one episode should be seen by the on call medical team. Investigations should be ordered after the patient is reviewed by the on call consultant. If the on call consultant agrees that they have had a TIA, these patients will need urgent investigations to rule out a high grade carotid stenosis. These patients would ideally have a CT Brain and CT Angiogram of carotid vessels on Friday / Saturday and if a ≥50% stenosis of the carotid artery is found, they are to be discussed with the stroke on call at St George’s for potential carotid endarterectomy. These patients will need to be transferred across to the Hyper-acute stroke unit.
Low risk TIA patients Patients presenting with ABCD2 score <4 need to be seen by a specialist within a week presenting to a health care professional and these individuals should be referred to the TIA clinic for further investigations. These patients will not require out of hours scanning.