Clinical Neurology

Module 1: Identifying ischemic locales

Module 2: Stroke
Key Neuroanatomical Structures for this module:

 Vasculature: ACA, MCA, MMA

 Meninges
 Ventricular systems and choroid plexus
 Broca’s, Wernicke’s areas
 Anterolateral Column Sensory Pathway (“Spinothalamic”, pain and temp. modality)
 Posterior Column Sensory Pathway (“Posterior”, vibration and proprioception)
 Occipital lobe and occipital radiations
 Visual fields in anterior frontal lobe
The case of Natasha Richardson, Epidural Hemorrhage:

 45F, fall during skiing

 Initially well, refused medical treatment
 Developed headache and confusion a few hours later
It is most likely that this unfortunate incident caused damage to the temporal bone, which is a relatively
soft bone in comparison to the rest of the cranium. Below the temporal bone, is the Middle Meningeal
Artery, damage to which probably caused an epidural hematoma, which given time to accumulate, exerts
pressure on the cortex and can lead the brain herniation. Brain herniation from a epidural hematoma, is
likely to be in the Uncal (uncus) location, (‘uncal herniation’) and therefore pressure the brainstem into
displacement, disrupting all the essential nervous
pathways and leading to death.
An epidural hemorrhage/hematoma should be
treated immediately and suspected from an early
stage to treat effectively. Often known as the
‘talk and die’, this kind of hemorrhage presents
as a lucid period, a clean neuro exam and is
often followed by rapid death.
It can be treated by Trepanation, or ‘burr holes’,
during which a screw-driver is used to create
holes in the cranium, allowing the excess blood
to leave and relieving pressure on the brain.
Bacterial Meningitis:

 Bacterial infection of the spinal or cortical meninges

 Patient placed in fetal position and CSF sample drawn from L3-L5 (location of cauda equina), sample
sent for analysis, and treated accordingly, typically with antibiotics.
Presentation:
The danger of
meningitis lies in its
ability to damage the
sub-arachnoid
granulations and
prevent the
reabsorption of CSF,
leading to
hydrocephalus.

Hydrocephalus: CT scan showing Lateral ventricular swelling causing pressure on the cortex from the inability
of the arachnoid granulations to reabsorb CSF, exerting pressure on the cortex.
Hydrocephalus:

Hydrocephalus can be either:

 Communicating (non-obstructive): appears symmetrical, caused by lesion in arachnoid granulations,

often caused by meningitis or post-meningitis scarring to the arachnoid matar.
 Non-communicating (obstructive): appears asymmetrical, caused by tumour or mass blockage, most
commonly caused by cerebral aqueduct blockage.
Stroke Presentation, a Clinical Application:
Rapid Neural Exam, ‘the 12P’s’:

 Psychological
 Pupils: size, symmetry, reaction
 Paired ocular movements
 Papilledema
 Pressure (BP)
 Pulse and rate
 Paralysis
 Pyramidal signs (spasticity, reflexes, Babinski reflex)
 Pin prick sensory response (anterolateral sensory)
 Pee
 Patellar reflex
 Ptosis (eye-lid droop)
Case Study:

 57M, right-handed, neck-pain, sudden onset neural deficit (sudden onset indicates stroke)
Presented with:
1. Aphasia
2. Right face, leg and arm weakness
3. Right face, leg and arm numbness
4. Cannot see right visual field
5. Deviation of eyeballs to the left
(Note: Aphasia = Broca’s, Dysarthria = Wernicke’s)
Distinguishing Locales:
1. The Broca’s area can be in different sides of the brain in different people, but handedness can indicate
which side (95% of right-handed adults have the Broca’s in the left hemisphere, whilst 73% of left
handed adults have the Broca’s in the right hemisphere). This patient is right handed, so we can safely
assume the problem is in the left hemisphere.

2. Weakness of right limbs and face could be either hemisphere, however, based on the handedness and
aphasia, we can assume that the damage is on the left. We can also assume left hemispheric damage
as hemispheres control opposite sides of the body due to pyramidal dessucation of the corticospinal
tract.
- (Upper neuron damage = distal muscle weakness, for example, extensors being weaker
than flexors, presenting as ability to squeeze fist but not extend fingers/open palm, or
ability to ‘close’ elbow, but not extend arm)
- Due to cell bodies of the pre-central gyrus being organized and corresponding with
amount of motor control, the area of impairment can also indicate the size and location of
stroke. Note that entire primary-motor cortex stroke is extremely rare, and complete right
side paralysis isn’t present, therefore we can assume that the problem is in the posterior
limb of the internal capsule.
3. Numbness could be due to either spinothalamic or posterior column sensory pathway. So, numbness
could be a result of injury to the post-central gyrus, however that is extremely rare and the previous
two presentations indicate a more cerebral location, presumably the thalamus.
- Note that the spinothalamic pathway is less myelinated, resulting in slower transmission
and delayed response.
- Posterior column: pin prick test
 4. Loss of right vision to the right side could indicate damage to occipital lobe or occipital radiations.
Assume optic radiations due to posterior location of occipital lobe being contradictory to previously
indicated locales.

5. Deviation of eyeballs to the left indicates damage to right hemisphere as each hemisphere ‘pushes’
eyes in opposite direction, i.e. the left hemisphere pushes eyes to the right, so when injury occurs to
the left hemisphere, the ‘right hemisphere wins’ and the eyes deviate to the left.
Conclusion:
All five presentations indicate ischemia to a left hemispheric cerebral location, ,most likely the posterior
internal capsule and surrounding structures. Note that images are NOT FROM THIS PATIENT.

Cause:
- Carotid of the anterior neck supplies the anterior 2/3 of the cortex
- Veterbrals supplies posterior cortex supplies posterior 1/3 of the cortex
Patients injury is in the territory of the MCA:

Neuroimaging techniques used: (images NOT from patient and may not be consistent): CT and angiography CT.

Diagnosis and Treatment: acute ischemic stroke of internal capsule resulting from embolus/dissection of the
anterior carotid. Treated with blood thinners. (Incomplete recovery)
Classification and Clinical
Presentation of Stroke
Stroke:

 Acute onset
 24hrs + neurological presentation
 Vascular mechanism
Transient Ischemic Attack (TIA):

 Clinical presentation of neurological symptoms <24hrs

Vessels:

0.5-1mm Usually cerebral MCA, PCA

<0.5mm Important small vessels (perhaps Thalamogeniculate,
feeding to internal capsule or lenticulostriate, arterial branches
thalamus) to the brain stem

Epidemiology:

 Decreasing among affluent, increasing among lower socioeconomic groups; showing preventability
 Leading cause of death in many countries (4th in UK)
 Men at higher risk than women but women at higher risk of mortality from stroke
Risk Factors:

 Age
 Asians at higher risk of intercranial hemorrhage
 Diabetes
 Hypertension
 Smokers (large vessel)
 Atrial-fibrillation leading to cardioembolic stroke
Prevention:

 Treat atrial-fibrillation with anticoagulants (prolog clotting time). Could also treat AF with warfarin,
dabigatran or oral factor Xa, but these are higher risk for cardio infarction.
 Treat high cholesterol with statin drugs (HMG-CoA inhibitors – lower lipids)
 Treat hypertension with weight loss and medications
Hemorrhagic Stroke
Hemorrhagic strokes represent around 15% of all strokes, and present as intracranial or intraparenchymal
bleeding. They very often are caused by aneurysm rupture, or small blood vessel rupture due to vascular
malformation, conditions such as amyloid angiopathy, transformation of ischemic stroke, or use of stimulant
drugs.
1. Aneurysmal: dilation or rupture, usually in thalamus/basal ganglia/pons/cerebellum. Usually 60+, can
be 40 with chronic hypertension.
2. Amyloid Angiopathy: amyloid proteins deposited on walls, linked with Alzheimer’s, usually in lobes,
not cerebrally.
3. Drugs or vascular malformation: usually young people
Somewhat counter logically, these kinds of strokes are not effectively treated by surgical removal of
hematoma, but rather, control of intercranial pressure, draining of CSF of lateral ventricles and protecting
airways to prevent aspirational pneumonia.
A subarachnoid hemorrhage typically arises from rupture of a berry aneurysm near branches of major
cerebrals, caused by blunt head trauma or pressure from other compartments. In which case the aneurysm
would be urgently clipped (intracranially) or coiled (endoscopically via femoral).
Aneurysms

 Congenital or from acquired weakening of the arterial walls from smoking or high BP.
 25% die at home, 5% invisible on CT
 If symptomatic can present pain from arterial stretch, especially within the territory of the trigeminal
nerve. May also cause pressure on brain parenchyma causing focal signs or pressure on Oculomotor
nerve, presentation as pupil dilation or diplopia. Note that the CT will be clear so the neuro exam is
IMPORTANT.

 Diagnosis of an aneurysm:
- Lumbar puncture to check color of CSF (yellow from conversion of hemoglobin to bilirubin)
- Sudden onset
- Loss of consciousness
- Arterial angiogram
Ischemic Infarction (small vessel):
Ischemic small vessel stroke accounts for 85% cases and typically arises from occlusion due to emboli. Small
vessel ischemia commonly occurs in the lenticulostriate arteries, brainstem penetrating arteries or as
lacunar syndromes (“little lakes’) and are typically caused by chronic hypertension which leads to lipid
hyalinosis.
Note that pure sensory strokes typically occur in the thalamus, in the Thalamogeniculate vessels arising
from the PCA, and motor strokes typically occur in the internal capsule contralaterally to the weak side.

 Tend not to rupture but rather ‘be clotted off’

 Hypertension high risk factor due to ‘coiling’ of vessels
 Can be pure motor: lacunar stroke, leaves contralateral weakness
 Can be pure sensory: thalamoperforator

Prevention of ischemic strokes:

 Aspirin (administer 200mg immediately) to inhibit platelet function

 Aggressive treatment of hypertension
 BP lower than 130/80 mm Hg
 Plasminogen activator administered within 3hrs of stroke (activates enzyme that breaks up plasma
proteins which cause clots)
Ischemic Infarction (large vessels):
  Thrombotic origin is uncommon, not as severe and can results from internal carotid atherosclerosis.
They tend to happen slowly over time and the circle of Willis compensates for the blood loss in the
area.
 Embolic origin is most commonly caused by AF, due to its dilation and clot formation within cardiac
vessels, but also from the internal carotid bifurcation, in which plaques are thought to occur from
endothelial injury and if ruptured can travel to the intracranial vessels.

Cardioembolic Artery-Artery
Atrial fb Carotid bifurcation atherosclerosis
Acute myocardial infarct Arterial dissection
Mechanical heart valve Aortic arch atherosclerosis
Bacterial endocarditis Intercranial atherosclerosis
Marantic endocarditis (lesions on prev.
undamaged heart valves)

MCA: lateral surface, partial frontal, parietal and Aphasia (Broca’s)

temporal
ACA (anterior cerebral) :‘follows’ cingulate sulcus,
limbic lobe and cerebrally located structures
PCA (posterior cerebral): occipital and parietal
Basilar: most severe because of supply to pons
and midbrain surface.
Neglect, confusion of unawareness of half of body
(spot cross test)
Hemiparesis: F = A > L, pronator drift
Gaze preference/deviation, optic radiations
Homonymous hemianopia (blindness of field)
Leg weakness contralaterally
Possible cognitive impairment
Homonymous hemianopia
Amnesia from hippocampus
Coma – rapid symptom
Cranial nerve palsies (ex CN3 diplopia)
Apnea – interruption of medulla
Cardiovascular instability – interruption of
brainstem

Transient Ischemic Attack:

 Indicative of future attacks

 ABCDD score (age, BP, clinical symptoms, duration, diabetes)
TIA’s are classified as presenting with neurological deficit symptoms for less than 24hrs, but in most cases they
last only around 30 minutes, so by the time the clinician is reached the symptoms have often ceased, which is
why taking a detailed history and using an advanced neuroanatomical knowledge to access which vessel was
occluded is of such importance. A large vessel TIA is typically an embolic occlusion, where as a small vessel
TIA is typically thrombotic (blood clot). For example, a patient that presents with temporary blindness or
amaurosis fugax maybe have suffered TIA from embolic occlusion of central retinal artery, or ipsilateral
carotid bifurcation.
Stroke Treatment:

 angiotensin enzyme convertors: make BP normal or slightly elevated to help collateral flow
 prevent hypoxic insult to injury or aspirational pneumonia by protecting airways
 physiotherapy
 embolectomy procedure
 vascular stent procedure: balloon angioplasty)
 administer rt – PA (catalyzes breakdown of plasminogen to plasmin) within 4.5hrs endoscopically via
femoral (better for large vessels)
Stroke Prevention:

 surgical removal of atherosclerosis plaques from carotid bifurcation

 oral anticoagulants for AF
 dabigatran (thrombin inhibitor, thrombin activates procoagulants)
 apixaban and rivaroxaban are oral Xa inhibitors but are associated with higher rate of myocardial
infarction.
 Aspirin
 For contraindication of aspirin: clopidogrel or Aggrenox (aspirin + dipyridamole, bv dilator)
Further Notes and Categorizations: