PBL 2- Sub Arachnoid Haemorrhage Flashcards
Difference Between Pain and Nociception
Pain:
- Perceptual phenomena - The consequence of Nociception - A subjective feeling - Defensive mechanism
Nociception:
- Signalling in the nervous system resulting from tissue damage
You can have tissue damage/nociception without pain/psychological distress
What are Mirror Neurons?
Activated by watching another person experience something
What are the steps involved in detecting nociception?
1) Origin of nociception is the process of tissue damage
2) Local effects and Signal generation - Leads to local effects (axon reflex) - Nociceptors convert mechanical or chemical signals into afferent neural action potentials 3) Transmission - Ascending neural pathways to the brain 4) Perception and emotions from higher centres 5) Antinociceptive signals sent back down - intrinsic opioid compounds
What is the Axon Reflex?
- Release of chemical mediators from local axon terminals
- Activation of immune system locally
- Degranulation of mast cells
- Arteriole dilation
- Smooth muscle contraction
- Plasma extravasation from nearby vessels
What are the different types of Pain receptors?
3 Classes of pain receptors
- Thermo - Chemo - Mechanical (associated with sharp prickling pain) - Polymodal ( acitvated by a variety of stimuli and found in almost all tissues)
What substances activate Nociceptors?
Alogenic chemicals include:
- Potassium (from damaged cells) - Serotonin (From Platelets) - Bradykinin (From Plasma) - Histamine (From Mast cells) - Prostaglandins (From damaged cells - arachidonic acid) Capsaicin (From chilli- has their own receptors)
What is the Nociceptor Reflex?
- Motor action performed automatically without involvement of consciousness
- Nociceptive information enters the Dorsal Horn of the spinal cord
- Information decussates as normal to the ascending pathway to the brain
- Some synapses in the local interneurons in the anterior horn to facilitate movement
- In the Anterior spinal cord there are alpha motor neurons that control skeletal muscles
This allows for motor movement that will remove the body part from the nociceptive stimulus.
How does Pain information get to the brain?
- Nociceptive information gets to the brain via the Spinothalamic pathway
- Initial stimulus is detected by terminal nociceptors
- This then travels through the Dorsal Root Ganglion
- Enters the spinal cord through the dorsal horn
- Synapses with the second order Neuron in the dorsal horn of the spinal cord
- Second order neuron decussates immediately to the anterior contralateral side of the spinal cord
- Ascends via the spinothalamic pathway to the brain- reaches the thalamus and also branches to the amygdala
- The 2nd order neuron synapses with the 3rd order neurone in the thalamus
The 3rd order neuron then takes the information to the somatosensory cortex (post central gyrus)
What is the Paleospino thalamic Pathway?
What type of pain does it produce? What type of fibre does it use? What Neurotransmitter does it use? What is the localisation of the pain? Where does it project the nociceptive information to in the brain?
Paleospino-thalamic pathway
Type of pain:
Produces aching, dull or burning pain
Type of Pain Fibre:
Travels via C fibres to DEEPER dorsal horn of spinal cord
Neurotransmitter:
- Transmits via substance P (slow sustained action)
Localisation:
- Passes to brain and produces poorly localised and usually distressing pain
Location in the brain and outcome:
- Most go to reticular formation, and then to the thalamus - producing increased alertness and arousal
The Neospino thalamic pathway
What type of pain does it produce? What type of fibre does it use? What Neurotransmitter does it use? What is the localisation of the pain? Where does it project the nociceptive information to in the brain?
Neospinothalamic pathway
Type of pain:
Produces Sharp, pricking pain from mechanical and fast thermal nociceptors
Type of Pain Fibre:
Travels via A delta fibres to the SUPERFICIAL dorsal horn of the spinal cord
Neurotransmitter:
- Transmits via Glutamate (Rapid and precise action)
Localisation:
- Passes to brain and produces well localised painful stimuli
Location in the brain and outcome:
- Most go to Somatosensory cortex and produce highly localised sensations
What is the Periaqueductal gray?
Where is it located?
What is its function in relation to pain?
- It is the gray matter located around the cerebral aqueduct within the tegmentum of the midbrain
- Receives information from the hypothalamus or limbic cortex regarding pain
- functions as an inbuilt anti nociceptive system to produce endogenous analgesics
- Has enkephalin producing cells that secrete in response to pain and act as a suppressant
- Projects to the Nucleus raphe magnus via the pontine noradrenergic neurons
Endogenous opiods are released
Explain Nociceptive pain
What stimulates it?
Is inflammation present in the cns?
Is it adaptive?
- No nervous system lesion or CNS inflammation
- Stimulus dependent pain
- Adaptive- protects by signalling potential tissue damage
- Has physiological stimuli such as mechanical, thermal or chemical
Explain Inflammatory pain What stimulates it? Is inflammation present in the cns? Is it adaptive? What can cause it?
- Active inflammation is present
- Can be spontaneous pain or stimulus dependent
- Can be evoked by stimulus that is usually not pain producing (light touch)
- It is adaptive and reversible - protects itself by producing hypersensitivity during healing
- Has peripheral and central amplification through inflammtory mediators
- Caused by : surgical inflammation, tissue trauma, joint inflammation
Explain Dysfunctional pain What stimulates it? Is inflammation present in the cns? Is it adaptive? What can cause it?
- No known structural nervous system lesion or active peripheral inflammation
- Spontaneous as well as stimulus dependent pain
- Present even with a lack of stimulus
- It is maladaptive and potentially persistent
- Caused by :
○ Fibromyalgia - sensitization of CNS nociceptive pathways
Primary Erythermalgia- mutation in Na channel leads to increased excitability of nociceptors
Explain Neuropathic pain
What stimulates it?
Is inflammation present in the cns?
Is it adaptive?
- Nervous system lesion or disease is present
- Marked neuroimmune response
- Spontaneous as well as stimulant derived pain
- There is sensory amplification maintained independent of the disease
Commonly perisistant and maladaptive
Explain Phantom pain
- Perception of pain in an absent limb
- Possibly due to activity in severed nerves
What is referred pain?
- Perceived at a site different from its origin
Innervated by the same spinal segment
What systems regulate motor control?
- The local spinal cord and brainstem circuits (LMR pathways)
- Descending Upper motor neuron pathways (UMN)
- Basal Ganglia (releasing inhibition on motor cortex)
Cerebellum (correction and fine tuning of movement)
Lower motor Neurons
What is the general function of a LMN?
what is the role of alpha versus gamma LMN?
- LMN activation always triggers contraction
- Alpha motor neurons innervate extrafusal fibres
- Gamma motor neurons innervate intrafusal skeletal muscle spindles
- 30 x as many interneurons as Lower motor neurons
- One LMN innervates a single motor unit which would consist of one or 20000 muscle cells
The motor unit size determines movement precision
What is a motor unit?
- The alpha motor neuron and the muscle fibres that it innervates
- May be large ie quads with 2000 muscle fibres
Small= eye muscles have 4-6 muscle fibres
- May be large ie quads with 2000 muscle fibres
Somatotopic Oranisation of the ventral horn Lower motor neurons
- Proximal muscles are represented in the medial spinal cord- anterior corticospinal tract
- Distal muscles are represented in the lateral corticospinal tract
Upper Motor Neurons Where is the cell body? Where is the target? Where are they found Where do their tracts go?
- Have their cell body in the CNS
- Target is also within the CNS
- Found in the motor cortex and the brain stem
Descending tracts
What is a Sub-arachnoid Haemorrhage?
• Bleeding into the subarachnoid space
○ Between the pia and arachnoid layer
○ Where blood vessels and CSF is located
What is the cause of the bleed?
Aneurysm on a blood vessel in the Sub arachnoid space ( 70%)
• Unknown (15%)
• Arteriovenous malformation
• Rare cases- tumour bleeding
What increases your risk of SAH?
- Female gender
- 3rd trimester of pregnancy
- Middle aged
- Abuse of stimulant drugs
- Connective tissue disorders
- Family history
- PCKD
What causes aneurysms to form?
- Defects in the media of the arteries
- Defects are thought to expand as a result of hydrostatic pressure from pulsatile blood flow and blood turbulence
- This is greatest at arterial bifucations
What causes aneurysms to rupture?
Related to the tension in the aneurysm wall
• Rate of rupture is directly related to the size of the aneurysm
• 5mm or less have a 27% risk of rupture
• 6-10 mm have a 40% risk of rupture
How does a SAH present?
What causes the symptoms?
Symptoms: • Thunderclap headache • Small leak may only produce minor headache • Reduced consciousness • Meningism ○ Vomiting ○ Neck stiffness ○ Photophobia • Seizures
Mechanism of symptoms: • Blood leaking from the aneurysms ○ Headache and meningism • Local pressure effects • Associated ICH and mass effect • Emboli
What signs would be associated with an anterior communicating artery aneurysm?
- Visual symptoms due to optic chiasm compression
- Positive Babinski sign
- Bilateral lower limb paresis
What signs would be associated with a Middle Cerebral artery aneurysm?
- Contralateral hand and face paresis
- Contralateral visual neglect
- Aphasia (dominant)
What is the work up for sudden onset severe headache?
• ABCs • History- ask about anticoagulants • Routine bloods and coag (group and hold) • IV access • Non sedating analgesia and hold any anticoagulants • Examination • Keep fasting • Investigations ○ CT Brain non contrast § Blood on CT = SAH § If no blood then do LP ○ CT/MRA Circle of WIllis +/- Digital subtraction cerebral angiogram § To find location of aneurysm • Angiogram and coiling if possible • If not suitable then for craniotomy and clippling • Chart ○ Nimodipine- for vasospasm ○ Fluids ○ Anti-seizure medication • Monitor GCS
How can you tell which vessel has the aneurysm on CT?
• blood in the Basal cisterns ○ COW aneurysm • Blood in the sylvian fissure ○ ICA, Posterior communicating or MCA • Interhemispheric or intraparenchymal ○ Anterior communicating artery
When should LP be performed?
• No need if there is obvious blood on the CT
• If there is a negative CT
• Should only be performed after 12 hours of headache onset and if raised ICP has been ruled out
○ It takes 12 hours for oxyhaemoglobin to be converted into bilirubin in the CSF
What are the complications of SAH?
· Re-bleeding
o 80% mortality if they re-bleed
o Minutes to 3 weeks after - Greatest risk is in the first 24 hours
o Aim to prevent this by controlling BP an isolate the aneurysm from circulation
· Hydrocephalus
o Communicating
§ Due to blood blocking reabsorption of CSF through the arachnoid granules
o Obstructive
§ Blood enters the ventricles and can block flow of CSF at the aqueduct or outlet of the 4th ventricle
o Need to have an external ventricular catheter through the right frontal lobe
· Vasospasm
o Blood vessels go into spasm causing ischaemia- stroke
o Suspected with deteriorating GCS/new neurological deficit
o Greatest risk of vasospasm is 4-7 days but is still significant for 3 weeks after the bleed
· Hyponatraemia
o Susceptible due to fluid loading and cerebral salt wasting
§ Renal loss of sodium to due intracranial pathology
· Seizures
o Blood is an irritant to the cortex and may spark a seizure
o Can give prophylaxis phenytoin or levetiracetem
· VTE
Due to bed rest
What is the main cause of stroke?
· Most ischaemia
· 20% intracerebral bleeds
· 5% SAH
What type of aneurisms is the most common?
Where do they occur?
· Saccular aneurysms
· Points of bifurcation in the circle of Willis
o Anterior communicating artery
o Posterior communicating artery
What is the first line investigation for SAH?
· CT non contrast
What is the pathogenesis of Bacterial Meningitis?
- infection of the upper respiratory trat
- Invasion of the blood stream (bateraemia)
- Crossing into the blood brain barrier
- Seedling and inflammation of meninges
- Bacterial capsule, specific surface receptors and ezymes
What are the clinical features of Meningitis?
- Fever
- Irritability
- Lethargy
- Poor feeding
- High pitched cry, bulging AF
- Convulsions, opsithotonus
- Stiff neck
- Photophobia
- Vomiting
- Drowsy
- Rash
What Positive clinical tests are suggestive of Meningitis?
- Kernigs sign
* Brudzinskis sign
What are the signs of Septicaemia?
- Rash
- Fever/vomiting
- Cold hands and feet
- Shivering
- Rapid breathing
- Stomach/joint/muscle pain
- Drowy/less responsive
What is the most common CNS infection especially in children < 1 year?
• Viral meningitis
What are the common bugs causing acute meningitis?
• 80% are due to:
○ N.Meningitidis
○ Streptococcus Pneumoniae (most virulent and fatal)
○ Haemophilus influenzae type b (falling due to vaccine)
• Listeria monocytogenes
○ Infants, elderly, immunosuppressed, cancer, alcoholism
• Staph Aureus
○ Head injury or nerusurgery
• GBS and Ecoli
○ Neonates
What are the causes of Chronic Meningitis?
• Lower virulence bacteria
• Slow growing bugs- TB
• Fungi - cyrptococcus
Incompletely treated pyogenic infections
What pathologic findings are seen in chronic meningitis?
- Granulomas
- Chronic inflammation
- Superficial Cerebral infarction
- hydrocephalus
What CSF findings will you see in meningitis?
- Increased protein
- Decreased glucose
- Increased white cells with increased neutrophils
What type of infection causes Encephalitis?
• Virus is the most common cause
