GEP (Life control) Week 3 Flashcards

1
Q

What are the 3 main movement pathways

A
  • Corticospinal (pyramidal) tract:
    Carries the messages from brain to peripheral nervous system
    Damage = weakness (paresis) or full paralysis
  • Extrapyramidal system (basal ganglia):
    Acts as a checkpoint to begin voluntary movement
    Modulates speed and smoothness of movement
    Underactivity = slow movement (bradykinesia), muscle rigidity, difficulty initiating movement
    Overactivity = uncontrolled involuntary movements
  • Cerebellum:
    Coordinates movements in space + learned motor patterns
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2
Q

What is the 3 main components of the brain

A

Cerebrum, Cerebellum and Brain stem

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3
Q

Identify the cranial fossass

A
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4
Q

What are the main 3 arteries that supply the cerebral cortex

A

Anterior, middle and posterior cerebral arteries -> form the Circle of Willis

Anterior circulation from internal carotid arteries:
Anterior cerebral artery
Middle cerebral artery

Posterior circulation from vertebral arteries
Posterior cerebral artery
* + cerebellum + brainstem

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5
Q

Describe the way that the Aneterior, middle and posterior cerebral arteries arise

A

Anterior circulation
Internal carotid passes through carotid canal
Loops back on itself then becomes the MCA
The ACA bificates of the MCA

Posterior circulation
Vertebral arteries pass through foramen magnum then come together to form basilar artery
Basilar artery works its way up the front of the brainstem (I’ll cover its other branches later)
Basilar eventually gives off the PCA which loops round to the back of the cerebrum

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6
Q

What are the territories within the cerebral cortex that each of the 3 main cerebral arteries supply

A
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7
Q

This is just a different view of the cerebral artery regions

A

the boarders of the cerebral arteries are not the same as the borders of the lobes in the brain

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8
Q

The MCA and PCA supplies which lobe of the brain that receives input from the macula (central vision)

A

The temporal lobe

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9
Q

What are the structures and functions of the cerebellum

A
  • Cerebellum is responsible for coordination in space as well as learned motor patterns
  • Middle of the cerebellum (vermis) handles coordination of the trunk and proximal muscles: important for posture (damage = truncal ataxia)
  • More lateral parts = coordination of the peripheries (damage = limb ataxia)
  • Flocculonodular lobe – linked to the vestibular balance system in the ear (damage = vertigo, nausea)
  • Unilateral cerebellar damage produces symptoms on the
  • ipsilateral (same) side
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10
Q

What are the cerebeller pathology

A

The best way to remember is DDANISH
There cerebellum coordinates movement in space through proprioception and visual input

Dysdiadochokinesia - inability to perform rapid, alternating muscle movements (finger tapping, opening and closing of fists etc)
Dysmetria - inability to judge distance
-Past-pointing
-Cerebellar rebound produces overshoot
-Difficulty focusing eyes on target
Ataxia - clumsiness.
-Cerebellar gait - usteady on feet, legs wide apart, veering towards side of cerebellar lesion
-Lateral cerebellar damage: limb ataxia (may also produce cerebellar gait)
**Nystagmus **- jerking of eyes. Eyes try to drift back to midline then jerk back to target
Intention tremor - involuntary, rhythmic muscle contractions (oscillations) that occur during a purposeful, voluntary movement.
Staccato speech (dysarthria - trouble speaking)
Hypotonia – low levels of muscle tone

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11
Q

What is the doll’s eye reflex

A

Cerebellum and brainstem connect the vestibular (balance) system in the inner ear to the occulomotor nerves
This produces the vestibulo-ocular reflex:
Turning the head one way produces reflexive movement of the eyes in the other direction so your gaze stays fixed on target
Loss -> ‘doll’s eyes reflex’ – where eyes move with the head

Loss of the vestibulo-ocular reflex is one of the signs doctors look for when confirming brainstem death
VO reflex can also be lost without brainstem death (vertigo etc)

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12
Q

What is the blood supply to the cerebellum

A

Basilar artery
Vertebral arteries
Superior cerebellar artery (SCA)
Anterior inferior cerebellar artery (AICA)
Posterior inferior cerebellar artery (PICA)

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13
Q

What is the blood supply to the brainstem and midbrain

A

The midbrain, pons and medulla oblongata are supplied by lots of tiny branches from the basilar artery and PCA.

These perforating/penetrating vessels:
Have tiny diameter, so vulnerable to blockage
Branch off at right angles (never a good design choice) so vulnerable to haemorrhage/damage

Damage to these tiny perforating vessels produces ‘lacunar’ infarcts –tiny areas of necrosis that leave small holes in the midbrain/brainstem
Usually lots of these have to accumulate over time
to produce serious symptoms

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14
Q

Desribe the venous drainage of the brain

A

Cerebral veins:
They lack muscular walls and valves
Empty into dural venous sinuses
NB: The cerebral venous system doesn’t follow arteries!

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15
Q

What are the main dural venous sinuses

A

Think of venous blood flowing from all points towards the confluence of sinuses posteriorly, then round and down to the internal jugular vein

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16
Q

What is a cerebral venous sinus thrombosis

A

CVST is when a thrombus occludes one of the dural venous sinuses, leading to accumulation of deoxygenated blood within the brain parenchyma -> cytotoxic oedema
DVT of the brain
CSF is also not able to drain
0.5-3% of strokes
Clinical features: headache, nausea, vomiting and neurological defects.

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17
Q

What is intracranial hemorrhage/haematoma

A

A hemorrhage refers to ongoing bleeding while the blood in a hematoma has typically already clotted.

There are 4 main types:
epidural Haemotoma
Intracerebral Haemotoma
Subcranial Hemorrhage
Epidural Haemotoma

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18
Q

What is an extradural haemorrhage

A

-Lentiform/lemon shaped
-Lemon-shaped because the periosteal dura, which should be attached to the bone of the skull, is torn away by the pressure of the haemorrhage (so only goes so far).

Classically caused by a rupture of the middle meningeal artery due to a skull fracture at the pterion – a weak point over the temple

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19
Q

What is a subdural haemorrhage/Haemotoma

A

-Crescentic/banana shaped
-Banana shaped because blood can fill the subdural space all the way until it is stopped by the falx cerebri at the midline
-Venous blood rather than arterial
-Classically caused by rupture of the veins that pass from the brain into the subdural space

20
Q

What is a subarachnoid haemorrhage

A

-Blood is between the arachnoid mater and pia mater, so closely follows the contours (gyri and sulci) of the cortex
-Most commonly due to a ruptured aneurysm in the Circle of Willis
-Dramatic onset
-“worst pain ever experienced”
-May cause meningism (photophobia, neck stiffness,
positive Kernig’s)

21
Q

What is a intracranial haemorrhage

A

10% of strokes are caused by intracerebral haemorrhage

Urgent CT to check for ICH is the first step in stroke management
Any stroke is ICH until proven otherwise because of the danger of giving anticoagulants to someone with ICH

The common sites of hypertension-induced intracerebral hemorrhage are the small penetrating arteries originating from basilar arteries or the anterior, middle, or posterior cerebral arteries.

22
Q

What is the circle of willis

A

The circle of Willis is an important junction of arteries at the base of the brain. The structure encircles the middle area of the brain, including the stalk of the pituitary gland and other important structures.

Two arteries, called the carotid arteries, supply blood to the brain. They run along either side of the neck and lead directly to the circle of Willis.

Each carotid artery branches into an internal and external carotid artery. The internal carotid artery then branches into the cerebral arteries. This structure allows all of the blood from the two internal carotid arteries to pass through the circle of Willis.

The structure of the circle of Willis includes:

left and right internal carotid arteries
left and right anterior cerebral arteries
left and right posterior cerebral arteries
left and right posterior communicating arteries
basilar artery
anterior communicating artery

23
Q

Give a quick overview on the production and function of the cerebrospinal fluid

A

Functions of CSF:
Support, shock absorber, homeostasis (pressure, waste, temperature), nutrition, immune function

Production:
CSF is made by the choroid plexus, mainly in the walls of the lateral ventricles (also 3rd and 4th ventricles).
The choroid plexus consists of pia mater, fenestrated capillaries, and ependymal cells (which make the CSF!)
Approximately 500ml is produced every day.

24
Q

What is the flow of CSF from the production to the subarachnoid space

A

Lateral Ventricle (x2) → Foramen of Monro (x2) → Third Ventricle → Cerebral Aqueduct → Fourth Ventricle

The CSF then enters the subarachnoid space via:
One of the two foramina of Luschka
→ cisterna magna → SA space
Foramen of Magendie
→ cerebellopontine cisterns → SA space
A small amount goes straight into the central canal of the spinal cord

25
Q

How is CSF removed

A

CSF is absorbed by arachnoid villi/granulations mostly in the superior sagittal sinus, where the most arachnoid granulations are. It then enters the cerebral venous system, following a pressure gradient.

26
Q

What are the main causes of raised intracranial pressure

A

Space-occupying fluid or mass
Meningitis
Encephalitis
Autoimmune inflammation e.g. multiple sclerosis
Bleeding
Tumours (a fairly uncommon cause)
Impaired/obstructed outflow
Obstructive hydrocephalus (complete CSF blockage)
Communicating hydrocephalus (partial CSF blockage reducing flow)
Venous thrombosis

27
Q

What are the consequences of raised CSF

A

Headache
Vomiting
Papilloedema (raised intraocular pressure)

If the cardiovascular system can’t compensate, cerebral perfusion drops
→ impaired supply of oxygen + glucose to brain → brain cell death:
Cell death adds to inflammation
Glutamate spills out of dead cells → excitotoxicity causes further damage to surrounding neurons
Ultimately, herniation of the brain downwards compressing the brainstem

Papilledema is a disease entity that refers to the swelling of the optic disc due to elevated intracranial pressure (ICP)

28
Q

What is the bodys response to raised intracranial pressure

A

Cerebral perfusion pressure = mean arterial pressure – intracranial pressure

As intracranial pressure increases, the sympathetic nervous system kicks in to raise arterial pressure to match it, so that blood can still flow into the brain (the Cushing reflex)

This means patients with a condition causing ↑ICP can have severe systolic hypertension

↑ICP in stroke, intracranial bleeding, hydrocephalus (CSF blockage), meningitis, cerebral inflammation/oedema etc.

29
Q

What occurs in the late stages of increased ICP after it is not treated

A
30
Q

What is a stroke

A

Stroke is an acute neurological deficit lasting more than 24 hours and caused by cerebrovascular aetiology :
intracerebral haemorrhage
subarachnoid haemorrhage
cerebral ischaemic stroke

31
Q

What are the differential diagnosis for stroke

A
  • Hypertensive encephalopathy (↑ICP)
  • Hypoglycaemia
  • Complicated Migraine
  • Seizure Disorder
  • TIA (Transient Ischaemic Attack, or ‘mini-stroke’)
  • Stroke symptoms which resolve within 24 hours.
32
Q

What is a great way to identify strokes

A

FAST:
Face
Arms
Speech
Time

33
Q

What are the different types of stroke

A

Haemorrhagic Stroke (13%)
Rupture of a cerebral blood vessel (venous or arterial), typically due to weakness in the vessel wall. Classified according to site of bleeding.

Ischaemic Stroke (87%)
Reduced blood supply and subsequent hypoperfusion to tissues, mostly due to thrombus within the cerebral arteries (e.g. secondary to atherosclerosis) or from an embolism, leading to infarction. The vessel affected largely affects the range of symptoms a patient will have.

34
Q

identify the Ischaemic stroke symptoms by vascular territory

A

ACA
-Motor and Sensory Cortices: Contralateral weakness and sensory loss
-Lower Limbs Affected
MCA
-Motor and Sensory Cortices: Contralateral weakness and sensory loss, visual field deficits, aphasia, agnosia, apraxia, agraphia
-Upper limbs and Face Affected
-Left Hemisphere: Aphasia (Broca’s and Wernickes)
-Right Hemisphere: Left-sided agnosia
-Occipital cortex: contralateral homonymous hemianopia

PCA
Occipital Lobe: Contralateral Homonymous Hemianopia
Note: If only one of MCA/PCA is affected, you get macular sparing due to dual blood supply
Posteromedial Temporal Lobes: Memory loss
Midbrain
Thalamus

Vertebral Basilar
Brainstem and medulla:
Cranial Nerve Disorders
Motor Deficits

Homonymous Hemianopia is a field loss deficit in the same halves of the visual field of each eye. This condition most commonly results from stroke for adults, or tumors/lesions for patients under the age of 18.

Aphasia is a language disorder caused by damage in a specific area of the brain that controls language expression and comprehension. Aphasia leaves a person unable to communicate effectively with others. Many people have aphasia as a result of stroke.

Agnosia is a rare disorder whereby a patient is unable to recognize and identify objects, persons, or sounds using one or more of their senses despite otherwise normally functioning senses.

Apraxia is a disorder of the brain and nervous system in which a person is unable to perform tasks or movements when asked, even though: The request or command is understood.

agraphia inability to write letters, symbols, words, or sentences, resulting from damage to various parts of the brain.

35
Q

How is strokes classified and what are the classification

A

Bamford/Oxford Stroke Classification is used to classify strokes

Total Anterior Circulation Infarct (TACS)
Involvement of both the ACA and MCA of the affected side
Unilateral weakness (contralateral hemiplegia/hemiparesis) Homonymous hemianopia (contralateral)
Higher cerebral dysfunction (e.g. aphasia, visuospatial neglect)
Partial Anterior Circulation Infarct (PACS)
Involves either the ACA or MCA of the affected side. Two of the TACI symptoms (or higher cerebral dysfunction alone)
Lacunar Infarct (LACI)
Subcortical stroke secondary to small vessel disease. There is no loss of higher cerebral functions, but one of: Pure sensory/motor or sensorimotor stroke, or ataxic hemiparesis.
Posterior Circulation (POCS)
Cerebellar/Brainstem signs.

36
Q

What is posterior stroke syndromes

A

These refer to sets of symptoms as a consequence of lesions in specific areas of the brainstem. This is more low-yield but get familiar with some of the names here.

37
Q

What are the investigations for strokes

A

First Line Imaging: Non-contrast CT Head
-Identifies haemorrhagic stroke
-Some changes can be seen for ischaemic stroke, however they tend to show up hours after the event:

Hyperattenuation (seen in acute emboli)
Hypoattenuation (infarcted tissue)
Loss of grey/white matter differentiation
Sulcal effacement
Loss of the basal ganglia (usually it’s first to go in an MCA stroke due to lack of collateral supply)
NOTE A normal CT scan dies NOT rule out ischaemic stroke, it’s a clinical diagnosis

Consider diffusion-weighted MRI Head if diagnosis remains uncertain despite radiology
-We don’t wait for an MRI if the patient has clinical signs and is
-within the thrombolysis/thrombectomy window.
Acute ischaemic infarct appears bright

38
Q

What is the management of Acute Ischaemic Stroke

A

-Give Aspirin ASAP (within 24 hours), continuing for 2 weeks

-Presentation within 4.5 hours AND thrombolysis non contraindicated: Thrombolysis with Alteplase
-You must ensure that Haemorrhagic Stroke has been excluded first.

-Presentation after 4.5 hours OR thrombolysis contraindicated: Offer mechanical thrombectomy with IV thrombolysis
-Confirmed occlusion of proximal anterior circulation (by CTA or MRA) within 6 hours
-If after 6 hours and within 24 hours of symptom onset, there must be evidence of salvageable brain tissue (CT or MRI)

39
Q

What is a headache and migrane

A

headache is pain or discomfort in the head or face. Headaches vary greatly in terms of the location and intensity of the pain, and how often the headaches occur. The brain tissue doesn’t have pain-sensitive nerve fibers and doesn’t feel pain. But, other parts of the head can be responsible for a headache including:

A network of nerves that extends over the scalp

Certain nerves in the face, mouth, and throat

Muscles of the head, neck, and shoulders

Blood vessels found along the surface and at the base of the brain

A migrane is a type of headache

40
Q

What are the 2 types of headaches

A
  • A primary headache means the headache itself is the main medical problem, although other factors, such as muscle tension or exposure to certain foods, may be identified. Other contributing factors include medicines, dehydration, or hormone changes.
  • A secondary headache is related to an underlying medical condition. An example of this would be a headache due to neck injury, eye problems, jaw, teeth or sinus infection.
41
Q

What are examples of primary headache disorder

A

Migrane
Most common cause of chronic headache episodes
Usually unilateral pain
Lasts hours to days if untreated
Patient wants to lay down in dark, quiet room
20% are accompanied by aura (usually visual) which precedes pain
Followed by tired, ‘washed out’ feeling

Tension Headache
“Tight band” sensation
Pressure behind eye
More commonly bilateral

Cluster Headaches (trigeminal autonomic cephalagia)
Headache episodes are close together, often happening nightly for 1-2 months but then a long gap
Unilateral
Excruciating pain behind the eye Management:
Analgaesics don’t work
Subcut sumatriptan + high flow oxygen acutely
Verapamil, lithium or corticosteroids may terminate the current cluster

Other primary headaches:
“Ice pick” headache
Primary cough headache
Others e.g. on urination, orgasm etc

42
Q

What are the managements for primary headaches disorders

A

Acute management of Migrane
Aspirin, paracetamol, NSAIDs
Sumatriptan (serotonin agonist)
Antiemetics (metoclopramide)
Chronic management of Migrane
Supression with antidepressants, anti-epileptics, beta blockers, ARBs

Tension headaches are managed in a similar fashion to migrane but added differences are:
Analgaesia for acute
Antidepressants first line for suppression (tricyclics)

Management Cluster headaches
-Analgaesics don’t work
-Subcut sumatriptan + high flow oxygen acutely
-Verapamil, lithium or corticosteroids may terminate the current cluster

43
Q

What is an analgaesic

A

An analgesic drug, also called simply an analgesic, pain reliever, or painkiller, is any member of the group of drugs used for pain management.

44
Q

What is Analgaesic overuse

A

-Most common cause of chronic daily headache
-Typically due to overuse of painkillers and/or sumatriptan
-Well-known progression from primary headache disorder e.g. migraine to chronic daily headache due to medication overuse
-Pain won’t resolve until patient cuts down/stops medications – tricky from a management and comm skills POV

45
Q

What causes secondary headache disorder

A

Idiopathic intracranial hypertension
Main worry is vision loss: ↑ intracranial pressure > ↑ intraocular pressure and compression of eye-related cranial nerves
Subarachnoid haemorrhage
Dramatic onset, worst pain ever, meningism, mortality+++
Extradural haemorrhage
Classic progression of head injury > period of recovery > sudden deterioration
Subdural haemorrhage/haematoma
Classically slower onset

46
Q

What is Broca’s area and Wernicke’s area?

A

**Broca’s Area: **Expressive dysphasia Difficulty with fluency of speech, getting the words out

**Wernicke’s Area: **Receptive dysphasia Difficulty understanding speech, resulting in normal fluency, but it’s a ‘word salad’.