PARA226 NOTES (PDF)

- 9. & 10 Glossopharyngeal & Vagus: Both motor & sensory functions including, sending sensory info from nose, throat, tongue & provides taste for back of tongue & voluntary movement for muscle in back of the throat. Originates in the medulla oblongata. Vagus nerve has both fun...

- 9. & 10 Glossopharyngeal & Vagus: Both motor & sensory functions including, sending sensory info from nose, throat, tongue & provides taste for back of tongue & voluntary movement for muscle in back of the throat. Originates in the medulla oblongata. Vagus nerve has both functions, including communication sensation info from ear canal & throat, sensory info from heart & intestines. Innervates the SA & AV nodes of the heart (when innervated slows down HR) & muscles in throat, chest & trunk & taste near root of tongue. Vagus has the longest pathway & originates in the medulla. - Have the patient open their mouth wide & say ‘aah’. Look at the uvula in the back of their throat as they do this. Their uvula should stay in a midline position. Ask the patient to swallow - they should be able to. - 11. Accessory: Motor nerve controlling muscles in the neck, allowing for extension, flexion & rotation. Spinal portion (supplies muscles in neck) & cranial portion (follows vagus nerve). - Have the patient turn their head to each side against resistance from your hand. They should have equal strength on each side. Alternatively, you might assess their ability to shrug by having the patient shrug their shoulders against resistance from your hands. The shrug should be strong & symmetrical. - 12. Hypoglossal: Responsible for movement of most of the muscles in your tongue. Originates in medulla oblongata. - Have the patient stick their tongue at you & see whether it stickers out straight, or to one side (abnormal) WEEK NINE: SEIZURES & STROKES Seizures: Defined as a temporary disruption of brain function caused by uncontrolled excessive neuronal activity. An electrical problem in the brain which manifests as altered sensations and/or activity in the body. - Maintenance of seizure activity requires a 250% increase in the demand of ATP in the brain - Cerebral oxygen demand increased by 60% - Cerebral blood flow increased by 250% As a result of these increased demands, oxygen and glucose supplies are readily used up & the patient may present hypoxic and hypoglycaemeic. Stages of a seizure: 1. Prodromus: - The period of time from the first symptoms to the full development of the seizure. Can be hours - days before a seizure. (difficulty sleeping, behavioural changes etc.) 2. Aura:  - The initial alterations in perception. Can be emotions, hearing, smell, taste or vision. Usually minutes to seconds before a seizure & is the first part. 3. Ictus: - The period of seizure 4. Post-ictal: - The state of confusion that lasts for minutes to hours after a seizure (not always present). - Can present with drowsiness, confusion, nausea, hypertension, headache, as well as fatigue, incontinence, fear & anxiety, trouble walking, hypoglycemia & tachycardia During the ictal phase, you can have these motor symptoms; - Tonus: sustained muscle constriction - Clonus: muscle jerking in a rhythmic way - Tonic-clonic: sustained contraction & then rhythmic jerking - Atony: muscle flaccidity - Trismus: tone/clenching of the jaw, restricting mouth opening In the post-ictal phase you can get Todd’s paresis: - Focal weakness in a part of the body, typically unilateral in the limbs. May also affect gaze, speech or vision & occurs in up to 13% of seizures (is a stroke mimic, so important to find out which came first) Seizures vs epilepsy: - Seizure: a transient occurrence of signs and symptoms due to abnormal excessive or synchronous neuronal activity in the brain - Epilepsy: a disease of the brain, defined as either: at least 2 unprovoked seizures occurring >24 hours apart, OR one unprovoked seizure and a high probability of further seizures. Can be considered resolved if there is an age dependent diagnoses/component & they have passed that age OR they have remained seizure free for the past 10 years with no seizure medications for the last 5 years. Acute symptomatic seizure; - Seizure occurring at the time of, or in close temporal relationship with, a central nervous system or systemic insult. Also known as reactive or provoked seizure. Seizures are a symptom of another event. Aetiology: - Cerebrovascular, trauma, CNS infection, withdrawal, metabolic, toxic, other - In >65 YO, cerebrovascular disease, such as strokes cause ⅔ of seizures  - Cerebrovascular disease: ischemia & hemorrhagic CVA/stroke, cerebral venous thrombosis, vascular malformation. - CNS infection: meningitis, encephalitis, cerebral malaria - Head injury: subdural haematoma, penetrating head injury, concussion, neurosurgery - Alcohol & medication withdrawal; suspected in pt with chronic abuse & occurs in 7-48 hours after last dose/drink - Metabolic: hypo/hyperglycaemia, hypo/hypernatremia, hypocalcaemia - Toxic: cocaine, antidepressants, antipsychotics, antihistamines, analgesics, alcohol intoxication (more common in overdose) - Other: eclampsia, febrile seizures, cerebral hypoxia Unprovoked seizure; - Occur in the absence of any precipitating factors or conditions. It is an inaccurate term as there are epileptic seizures that can be brought on by certain things such as light flashing lights or sleep deprivation, however it is not the sole precipitant. Epilepsy aetiology: - Genetic, structural, infectious, metabolic, immune, other - Genetic: a chromosomal or genetic abnormality (epilepsy from birth/young age) - Metabolic: genetic metabolic disorders eg. cerebral folate deficiency (epilepsy from birth/young age) - Immune; immune response causing central nervous system inflammation & is different from infectious, due to it antibody mediated. - Infectious: meningitis, encephalitis, cerebral malaria - Structural: CVA/stroke, TBI, tumours, vascular malformations, scarring from cerebral hypoxia Classification: - Created by the International League Against Epilepsy (ILAE) - Used to facilitate communication in clinical care, research & teaching Focal onset: unilateral, limited to one hemisphere at onset - Can be more discrete (more localised/unifocal) or more widely distributed & multifocal/hemispheric - Aware: the patient is fully aware of themselves & their environment throughout the entirety of the seizure - Impaired awareness: if awareness is impaired at ANY point throughout seizure - Motor: any ipsilateral tonus or clonus present (one side of the body) - Non motor:no motor activity, instead would present with sensory, cognitive, autonomic, emotional or behavioural arrest. - Interventions are required more heavily if the individual has impaired awareness at any point. - Jacksonian March: a focal motor seizure that has an orderly progression of seizure activity from the distal part of the limb toward the body, due to distribution of the anatomical areas in the primary motor cortex. Generalised onset: originating at one point then very rapidly progresses to bilateral involvement - Awareness is not used as classifies for generalised seizures as the vast majority have impaired awareness - Motor: For generalised motor seizures, motor activity will be bilateral from the onset - Specific descriptions of motor activity can described, but not required - Absent/non motor: present with sudden cessation of awareness and activity, tending to occur in younger patients & have a sudden start & stop. Usually display some automatic, non purposeful movements (lip smacking, hand movements) Focal to bilateral tonic clonic; - Starts unilaterally & then progresses to bilateral tonic-clonic movements Unknown onset: unknown if focal or generalised at onset - Onset of the seizure wasn't witnessed however further description explanation may be offered Unclassified: unwitnessed/all elements unknown - Nothing is known about the seizure, or it doesn't fit any of the other categories. Status epilepticus; Epidemiologically defined as: - A prolonged seizure >30 mins duration, OR - A series of seizures during which function is not regained between ictal events in a 30 minute period Clinically defined as: - >5 minutes of continuous seizure, OR  - >2 discrete seizures between which there is incomplete recovery of consciousness Status epilepticus is a life threatening emergency requiring immediate intervention with a mortality rate up to 20%. - Excitotoxicity & hypoxia are thought to the two main elements behind its fatality - Excitotoxicity: excessive exposure to the neurotransmitter glutamate ot overstimulation of its membrane receptors, leading to neuronal injury or death - Increased duration of status epilepticus worsens the prognosis, with neuronal injury becoming irreversible after around 30 mins - Refractory status epilepticus: when the seizure continues post benzodiazepine administration Assessment: Questions for the witness: - Description of the event & onset? - How long did their seizure last? - For generalised or focal impaired awareness seizures, the patient wont remember the details & will initially be confused in their post-ictal state. Questions for patient; - Any symptoms leading up to the seizure? Any prodromal symptoms, causes, triggers? - Was there an aura? Funny sensation prior? - Personal or family history of seizures? - Compliance with anti-seizure medication? - Triggers? Exhaustion, overstimulation, concomitant illness? - History of multiple seizures? Physical examination - Head trauma - Oral trauma eg. tongue biting - Incontinence - Fever/stiff neck (meningism) - Focal neurological deficits eg. altered sensation or motor weaknesses & what came first - Injuries / broken bones from contractions Differential diagnoses: - Syncope: cardiac, vasovagal, orthostatic - Psychological: dissociative states, psychogenic non-epileptic seizures, panic attacks - Migraines: visual auras, hemiplegia, vertigo - Paroxysmal movement disorders: tics, tourettes  - Sleep disorders: narcolepsy - Metabolic conditions: hypo/hyperglycaemic, hyponatremia, hypocalcaemia, hypomagnesemia, hyperthyroidism - Vascular conditions - Gastrointestinal conditions: esophageal reflux in neonates & infants - Traumatic: subdural hematoma, subarachnoid haemorrhage, TBI, brain abscess, meningitis, encephalitis Treatment: - First aid: recovery/side position, loosen clothing, avoid oral, - Protect the body during ictus - Airway patency: consider trismus, suction, NPA, oxygen - Benzodiazepines as required (midazolam IM 10mg, repeat once @5/60 if required) - The ILAE recommends pharmacological interventions should begin at the 5 minute mark - IV access if possible - MICA (IV midazolam, ETT) Treat & refer: If this is a typical, self limiting seizure and the patient has returned to normal baseline level of awareness, consider treat & refer if they are able to be monitored by a responsible adult. Do not proceed if: - Patient requires further in-hospital assessment/treatment (incomplete recovery, non epileptic cause, no diagnosis/first presentation, concurrent illness, midazolam administration, different to usual presentation) - Seizure was unwitnessed - Risk of recurrent seizure (history of multiple seizures, feeling of impending seizure, unable to be monitored by adult) - Pregnancy - Patient requests transport Strokes: Includes a group of disorders involving a sudden, focal interruption of cerebral blood flow that causes neurologic deficit. This interruption can be caused by a blockage (ischemic) or from a bleed (haemorrhagic). Neurological deficits can vary depending on which cerebral artery is affected and the area of the brain that artery supplies. Risk factors: - Age: ⅔ of strokes occur in >65 group & is 3x higher again in >85 - 1.4 times higher in males - Higher rates in the indigenous population - Tobacco smoking - Hypertension - Dyslipidemia - Previous transient ischemic attack - Atrial fibrillation - Diabetes Anatomy review: The blood vessels supplying the brain are two internal carotid arteries & two vertebral arteries - The carotid arteries contribute 80% of total cerebral blood flow Anterior circulation: - Anterior cerebral artery, middle cerebral artery & internal carotid arteries - Anterior cerebral artery: controls motor & sensory of trunk, hips, legs & genitals. - Middle cerebral artery: motor & sensory of hands, shoulders, arms, eyes, face, tongue as well as speech areas; Broca’s (expressive speech/output of speech = aphasia/dysphasia) & Wernicke’s (receptive  speech/understanding = comprehension of own & others speech) Posterior circulation: - Posterior cerebral artery & basilar artery (fed by vertebral arteries) - Posterior cerebral artery: visual cortex - Basilar artery: feeds cerebellum, controlling balance, and brain stem, controlling crucial functions - Vertebral arteries; feeds both posterior & basilar regions Ischemic strokes: An episode of neurological dysfunction caused by a focal CNS infarction - 87% of all strokes - Penumbra: the infarcted portion is known as the core or umbra. The surrounding area that is hypo-perfused and ischemic is known as the penumbra (the salvageable portion). Approximately 1.9 million neurons die per minute in hypo-perfused ischemic penumbra. Small vessel occlusion: Occlusion of the small cerebral arteries that supply the deeper structures of the brain (¼ ischemic strokes) - Predominantly caused by vascular pathologies: - Thickening of the artery walls & hypertrophy of the smooth muscle, narrowing the vessel - Atheroma & stenosis - Can technically be caused by an emboli, but is uncommon - Smaller vessels mean smaller infarcted core, however can still be fatal - S&S; - Hemiparesis: one sided weakness - Dysarthria: difficulty speaking with motor function - Altered sensation - Ataxia: discoordinated movements & trouble walking - Combination of sensory & motor Can be treated with thrombolysis, but efficacy depends on mechanisms behind the stroke Large vessel occlusion: (LVO) Occlusion of any of the large cerebral arteries/intracranial vessels, including the basilar artery (BA), the internal carotid artery (ICA) and the middle cerebral artery (MCA). Approximately 50% of ischemic strokes - Some definitions included posterior cerebral artery (PCA), anterior cerebral artery (ACA), and vertebral artery (VA). - Around 80% of LVOs affect anterior circulation - Causes include: - Primary atherosclerosis - Extracranial artery atherosclerotic embolism: atherosclerosis that shoots off an embolism, primarily in the lower arteries  - Cardioembolic events (atrial fibrillation): valvular disease, embolism from aorta - Cryptogenic (unknown) - Disproportionate contributor to mortality & morbidity. LVOs are responsible for 60% of post ischemic stroke dependence & death & 90% of post ischemic stroke mortality Can be treated with thrombolysis or endovascular clot retrieval (ECR) Anterior circulation strokes Posterior circulation strokes 75-80% of strokes 20-25% of strokes 91% FAST positive 60% FAST positive (more challenging to diagnose & more often missed) Common symptoms: Common symptoms: - Hemiparesis/hemiplegia (one side) - Vertigo - Altered conscious state - Headache - Ipsilateral sensory deficit (same side) - Ataxia - Facial palsy - Hemiparesis - Dysarthria - Blurred vision - Dysarthria Sensitive symptoms: specific to anterior Sensitive symptoms: specific to posterior - Aphasia (associated with eyes) - Gaze palsy - Nystagmus - Hemi-environmental neglect (usually - Oculomotor palsy left) - Horner's syndrome: drooping eyelid, miosis, facial anhidrosis - Diplopia - Quadrantanopia: quarter field vision loss Transient Ischemic attacks (TIAs): Transient episode of neurological dysfunction caused by a focal brain, spinal cord or retinal ischemia, without acute infarction - Stroke symptoms - Sudden onset - Typically only lasts minutes, but can last hours - Post TIA, the risk of stroke within 3 months has been reported to be around 20%, with 50% of those within 2 days All potential TIA patients must be transported to hospital. TIAs can't be diagnoses prehospitally, imaging is still required, and early intervention reduces the risk of stroke by 80% Haemorrhagic stroke: An episode of focal neurological dysfunction caused by a focal collection of blood in the CNS that is not caused by trauma  - 13% of all strokes - Poor morbidity & mortality (30 day mortality rate = 35-52%) Intracerebral haemorrhage: A focal collection of blood within the brain parenchyma or ventricular system - A bleed that it is the cerebrum area - ⅔ of hemorrhagic strokes - Substantial displacement of the brain parenchyma may cause elevation of ICP and potentially fatal herniation syndromes. The buildup of blood can push the brain across. - 50% will have an altered GCS, with overt GCS = worse outcome predictor - 50-70% wil have a headache & 6-7% will have seizures - Causes can include: - Chronic hypertension: puts pressure on vascular system & causes aneurysms which can burst - Cerebral amyloid angiopathy: condition where amyloid (protein) builds up on the walls of the arteries in the brain, which weakens the walls & makes them more susceptible to breaking - Anticoagulation medications - Vascular malformations - Secondary to ischemic strokes - Can be a gradual or sudden onset, depending on specific mechanisms/cause - S&S: depend on location of the bleed - Headache, nausea, vomiting, altered conscious levels, weakness or numbness, vision loss, seizures Subarachnoid haemorrhage: Bleeding into the subarachnoid space (the area between the arachnoid membrane and the pia mater of the brain or spinal cord) - ⅓ of haemorrhagic strokes - Patient typically presents with thunderclap headache, usually the worst headache of their lives & is often associated with photophobia & nuchal rigidity (blood surrounds brain & spinal cord, mimicking meningitis) - Almost 50% present with profound loss of conscious - Focal neurological deficits often present either at the same time as the headache or soon after - Causes include: - 85% due to aneurysm rupture (berry aneurysms) - 15% varied causes: include vascular malformations Treatment can include conservative treatment including BP & ICP control or neurosurgical decompression **ischemic strokes block a specific & localised portion of the brain, whereas a haemorrhagic stroke presents more with global symptoms due to the pressure build up of the blood on the brain (global symptoms & altered conscious / < GCS 8) Assessments: Stroke screening tools: - Face arm speech time/test (FAST) (public predictor for ischemic strokes) - National institutes of health stroke scale 8 (NIHSS-8) - Melbourne/metropolitan ambulance stroke screen (MASS) - HUNTER 8 - Field assessment stroke triage for emergency destination (FAST-ED) - Recognition of stroke in the emergency room (ROSIER) FAST: - Face: ask the person to smile & does one side of the face droop? - Arms: is one arm weak or numb? Raise both arms, does one drift downward? - Speech: is speech slurred? Is a simple sentence repeated correctly? - Time: Time of onset? Identified 70-90% of strokes, however missed up to 40% of posterior circulation More complex stroke assessments: - More details FAST (level of facial palsy, hemiparesis, dysarthria) - Level of consciousness - Eye assessment - Visual/sensory neglect or extinction - Modified Rankin scale: assesses the patient's premorbid function, if a high score, pt is unlikely to receive interventions Good measure of stroke severity, predict LVOs & lesion size Facial motor assessment: - Top half (above eyes) = bilateral innervation - Forehead wrinkling, brow movement, eye squeeze - Bottom half (below eyes) = unilateral innervation - Smile, nasolabial fold, tongue protrusion Facial palsy: - Partial palsy: unilateral lower face motor deficit - Complete palsy: unilateral upper & lower face motor deficit (likely to be a lower motor neuron affected = brain stem = posterior stroke OR stroke mimic such as bell’s palsy) Motor associated further assessments - Limb hemiplegia: can't move their limbs against gravity (can't lift limb up) - Limb hemiparesis: can't sustain limb against gravity (up to 10 seconds) - Dysarthria: difficulty speaking (due to loss of motor control) - Dysphagia: difficulty swallowing (due to loss of motor control)  - Gaze abnormality: restricted ocular motion past midpoint (H test) (one eye can't track past midpoint) Sensory associated further assessments - Dysphasia/aphasia: language difficulties (expressive or receptive) - Visual or sensory neglect: unilateral lack of response to stimuli (cant feel or see on certain side) (if you do it on one side, they cant feel/see that side & have complete neglect of that hemisphere) - Visual or sensory extinction: unilateral lack of response to stimuli only when both sides are stimulated simultaneously (can only feel/see one side when tested = extinction of one side when tested simultaneously Missed signs: - Vertigo - Diplopia: double vision - Ataxia: difficulty coordinating movements Lateralisation of the brain functions: Certain functions are only in one hemisphere - Language centres are more often in majority of patients in the left hemisphere (not all the time, but majority) - If you have right side motor deficit (hemiplegia) that is controlled by the left hemisphere, you might also see difficulties with language - If you have right hemisphere infarction, there will be left motor deficit, with right sided neglect Blood pressure: - 80% of stroke patients will present with hypertension, which can be due to dysregulation from injury, or compensation due to increased ICP - Any changes to systemic pressure can change the impact of expansion of the ischemic core (penumbra - core). If pressure is too low, the core might get greater, or if the pressure is too high, the haemorrhage might grow. If ICP pressure is increasing, in order to maintain CPP, systemic BP must increase, however if systemic BP is too high it can be contributed to poorer outcomes. - It also might change which intervention is available for the patient, so note changes to BP & handover this information. Cerebral perfusion pressure (CCP) = mean arterial pressure (MAP) - intracranial pressure (ICP) - CPP: pressure required to maintain cerebral perfusion - MAP: diastolic BP + ⅓ of systolic-diastolic - ICP: pressure inside your skull due to the rigid capsule preventing expansion. This increases with any oedema or intracranial bleeding. Stroke mimics: 1. Post ictal / seizures  - Todd’s paresis, gaze deviation, decrease levels of awareness - To rule out stroke: history of seizures, or seizure witnessed prior to stroke symptoms (whichever one came first) 2. Migraine: - Up to 25% of migraine sufferers will have focal neurological symptoms, & hemiplegic migraines exist. Most migraines are self resolving but some can suffer permanent neurological changes: - To rule out stroke: history of migraines & presents exactly like current presentation 3. Metabolic: - Dysglycaemia can cause hemiparesis. More common in HHS due to encephalopathy. Hypernatremia, hyponatremia, hepatic encephalopathy & thyroid storm may also cause focal neurological deficits. - To rule out stroke: BSL. Most stroke guidelines require normal BSL (if BSL is fixed & stroke symptoms remain = can rule in stroke) 4. Bell’s Palsy: - Temporary, unilateral paralysis of the face usually due to trauma or infection to the facial nerve (CN7) - To rule out stroke: good history taking, no other stroke symptoms, 5. Functional neurological disorder: - Presents with limb weakness, numbness, or speech disturbances - To rule out stroke: Clinical signs demonstrate inconsistency and reversibility (often through distraction) 6. Brain tumours; - Gliomas, meningiomas, adenomas 7. Cerebral infections: - Meningitis, encephalitis ** Err on the side of caution. If you cannot entirely rule a mimic in, a stroke must be considered. Treatment: 1. Early identification 2. Timely transport to appropriate hospital with notification (stroke unit & reperfusion therapies) - Monitor BP (too hypertensive might not be eligible for thrombolysis) - Consider: - Large bore IV cannula (imaging & medications in-hospital) - MICA for intubation of the unconscious patient (try not to delay transport) - Antiemetics to minimise gagging & vomiting (prophylaxis for ICP) - Treat seizures with benzodiazepines/midazolam - Oxygen in the hypoxic patient (high flow can be associated with worse outcomes of not required) Definitive assessment: Brain imaging: - Shows ischemic VS hemorrhagic - Aids decision of treatment pathway & timeline - Non contrast CT: shows haemorrhage & some mimics such as tumours (favoured & available, but not good at identifying posterior circulation strokes) - CT angiogram: contrast dye shows image of cerebral vessels, showing which artery is occluded during an ischemic stroke. - CT perfusion: measured cerebral blood flow & cerebral blood volume within cerebral tissues. Shows the penumbra & core of the stroke using dye. Definitive treatment Ischemic stroke: - Thrombolysis - Tenecteplase or alteplase are most commonly used. - Used in all ischemic stroke patients within 4.5 hours of symptoms onset. If CT perfusion imaging shows salvageable penumbra, thrombolysis can be administered up to 9 hours post symptom onset. - Less successful in LVOs, however, should be given in conjunction with ECR. - 6% of thrombolysis pts were at risk of ongoing haemorrhage which can form into haemorrhagic stroke = risky procedure but risk VS benefits. Why BP should be lower than 185. - Endovascular clot retrieval: - Technique where they enter the groin & femoral artery with a catheter & under x-ray they find the site of the clot, cross through the clot & capture it with a mesh cage, using vacuum suction to pull out & remove the clot. - Only able to treat LVOs & will be considered up to 24 hours post symptom onset. - Improved 90 day functional independent rates from 13-50%. - Only available at specific hospitals. Haemorrhagic stroke: - Conservative treatment: - Maintain balance of BP - Osmotherapy & hyperventilation can be trialled in those with oedema or increased ICP - BGLs kept in normal range (40 years) - Other associated conditions or features (head trauma, illicit drug use, toxic exposure, headache on awakening, precipitated by cough/exertion/sexual activity) - Previous headache history with progression or change in frequency, severity or clinical features Life threatening causes of secondary headaches: - Trauma to the head or neck - CVA or cerebral vasculitis - Tumours & increased ICP - Seizures - Medications or positions (Nitrates = vasodilation, carbon monoxide) - Infections (meningitis, encephalitis) - Hypertension, dehydration, renal or thyroid problems Treatment: - Gentle handling, reduce stimulus (lights, noise, sirens) - Non-narcotic analgesia (paracetamol) - Antiemetics (prochlorperazine) - Raise the head of the stretcher 30 degrees to help decrease ICP - Transport to a neuro centre if the patient has any red flags Neurogenic shock: Shock occurring in the setting of normal blood volume (normovolemic hypotension) - Refers to the haemodynamic instability that occurs in the setting of a spinal cord injury at the level of T6 & above, and is related to the  loss of sympathetic tone to the peripheral vasculature & heart - Significant loss of sympathetic division past T6, but large preservation of parasympathetic, leaving the spinal column much higher than the level of injury. The result being that the loss of sympathetic tone prevents the usual ability to control the peripheral vascular and increase the firing rate & contraction of the heart. - Involves the loss of innervation to the Celiac ganglion, which results in an inability to stimulate the adrenal glands to release catecholamines (adrenaline & noradrenaline) with resulting loss of vascular tone and decreased inotropy (contractility) & chronotropy (heart rate). Signs & symptoms: - Hypotension - Bradycardia (inability to mount a tachycardic response) - A possible sweat line (pale & sweaty above injury line and dry & flushed below injury line) - Hypothermia **not to be confused with spinal shock which is associated with lower body paralysis & anaesthesia & an absence of pain & the presence of unexpected calmness - (spinal shock) Dysfunction of the spinal with the loss of reflexes and sensory & motor function below the level of injury VS (neurogenic shock) the distributive shock & haemodynamic changes that are apparent in the spinal cord patients Treatment: - BLS & spinal immobilisation - Conservative fluid challenge to help support perfusion - Vasopressors (adrenaline, noradrenaline or dopamine infusion) (MICA) Autonomic dysreflexia: Uninhibited or exaggerated sympathetic response to noxious stimuli below the level of injury, leading to diffuse vasoconstriction & hypertension & severe headache - Usually occurs in patients with spinal cord injuries above T6 - Typical stimuli include bladder distension, bowel impaction, pressure sores, bone fracture, occult visceral disturbances or sexual activity - The parasympathetic activity that occurs when the rise in BP is detected by the baroreceptors in our carotid bodies & aortic arch results in a compensatory bradycardia & vasodilation above the injury, but is not usually unable to control hypertension that continues to escalate Signs & symptoms: - Normal SBP for an individual with a spinal cord injury above T6 is 90-110mmHg. An increase of 20-40mmHg above this can suggest the diagnosis, and it is not uncommon to see profound hypertension (>200) in AD. - Bradycardia is common, as well as pounding headaches, nausea, anxiety, blurred vision & nasal obstruction - Profuse sweating and flushing abode the lesion (often face/neck/shoulders), with goosebumps below the injury - The severity of attacks ranges from asymptomatic hypertension to hypertensive crisis continuing by profound bradycardia, cardiac arrhythmias or arrest, intracranial haemorrhage & seizures Treatment: - Monitoring of blood pressure - Positioning of patient upright to orthostatically lower blood pressure - Removal of tight fitting garments - Searching for & correcting noxious inciting stimuli - Bladder distension, pressure areas, wounds, ingrown toenails, fractures - Nitrates (GTN 300-600 mcg, repeat @ 10/60 intervals) Malignant hyperthermia: Though rare, it is a severe, life threatening, hyperthermic response to medications, usually triggers by the combination of an inhaled anaesthetic and a depolarising neuromuscular blocker Signs & symptoms: - Muscular rigidity, especially of the jaw (often first sign) - Tachycardia or other dysrhythmias - Tachypnoea - Acidosis - Shock - Hyperthermia, with temp usually >40, but can progress to extremes >43 - Hypercapnia, as detected by an increased EtCO2 - Urine may appear brown or bloody if rhabdomyolysis and myoglobinuria have occurred Treatment: - Stop causative drug - Aggressive cool the patient - Immediate transfer to hospital for dantrolene to stop the hyperthermia Extrapyramidal reactions: The pyramidal system:  - At the back of our brain are two medullary pyramids. Some of our motor tracts go through the pyramids (pyramidal tracts) & some do not (extrapyramidal tracts) There are 2 pyramidal tracts which both have neurons that start in the upper part of the brain (cerebral cortex). Some go from the brain to the cranial nerves to modulate facial movement via the corticobulbar tract & some go from the brain to large voluntary muscles & control body movement via the corticospinal tract The extrapyramidal tracts have neurons that start in the lower part of the brain (brainstem). These tracts control involuntary motor reflexes, walking & complicated movements (especially of our hands) and control our posture. Extrapyramidal reactions: serious neurological symptoms that may occur after initiation of antipsychotic drugs. - Drug induced movement disorders that are seen in patients taking antipsychotics & dopamine receptor blocking agents - Acute dystonia: - Manifests as involuntary muscle contraction & abnormal muscle posturing, affecting muscles of the neck, jaw, eyes, face & tongue, making it difficult to breath, swallow & speak - Occurs within hours of taking the medication - Treated with anticholinergics - Akinesia: Parkinson like syndrome - Collection of symptoms describing things like tremor, muscle rigidity, slowing of movements, changes of gait etc. & generally appear within a few days of taking the medication - Treated with dopamine agonists - Akathisia: - Inability to sit still & motor restlessness, leading to repetitive movements, usually of lower limbs, with leg crossing, swinging or shifting - Tardive dyskinesia - Manifests as involuntary, repetitive movements of the face & tongue - Occurs within months of the medication - Often permanent, not painful, but can cause difficulties chewing & talking Acute dystonic reactions: - Involuntary, sustained muscle contractions causing abnormal posture and/or repetitive twisting motions - Common causes included drugs, genetics, or for reasons unknown - Laryngospasms & failure of respiratory muscles are the most concerning short term features Management: - Anticholinergics, antihistamines, benzodiazepines & beta blockers are all used in various ways to treat these EP reactions - Most reactions are not immediately life threatening, however, reactions with laryngospasm or respiratory failure will require MICA (intubation & pharmaceutical treatment) - Benztropine is a drug made up of atropine & diphenhydramine used to treat acute dystonic reactions & is carried by most ICPs Neuroleptic malignant syndrome: - Severe & life threatening adverse drug reactions occuring with neuroleptic/antipsychotic drugs - Can be triggered by haloperidol Signs & symptoms: - Motor abnormalities: - Patients may have generalised, severe muscle tremor or rigidity (& less often, dystonias or chorea). Reflex responses tend to be decreased - Altered mental status: - Usually one of the earliest manifestations is a change in mental status, often an agitated delirium, which may progress to lethargy or unresponsiveness - Hyperthermia: - Temperature is usually >38 & often >40 - Autonomic hyperactivity: - Autonomic activity is increased, tending to cause tachycardia, arrhythmias, tachypnea, diaphoresis, labile BP (suddenly changes from normal to high) or hypertension Treatment: - Aggressive cooling - In-hospital management will usually involve medically supervised cessation of the causative drug & administration of dantrolene to stop the hyperthermia Parkinson's disease: Neurodegenerative disorder - Brain produces an aberrant protein that forms into permanent fibres, called Lewy bodies, which interfere with many functions of the CNS, including with the dopamine producing parts of the motor centres, which can lead to Parkinsons - Symptoms usually begin gradually & worsen over time  - Patients take a drug that is converted to dopamine in the brain (levodopa) along with a drug to help get the levodopa into the brain without being broken down (carbidopa) Signs & symptoms: - Bradykinesia: slowness of voluntary movements - Rigidity: increased resistance to the passive movement of a joint that impedes active & passive movement (cogwheel rigidity) - Akinesia: absence of & lack of control over voluntary movement - Tremor: appears at rest & during stationary limb positions - Postural abnormalities: inability to maintain an upright trunk position while standing or walking It is rare for Parkinsons to manifest as an acute crisis, however one of the most common presentations is due to orthostatic hypotension. - Fluctuations in drug levels can lead to an acute exacerbation of Parkinson symptoms - Sometimes patients can experience a severe, hyperpyrexic emergency with altered consciousness, severe rigidity & rhabdomyolysis, which can be fatal if not treated urgently - Patients can have acute psychotic episodes, especially with concomitant infections - Patients may have dystonic reactions due to the medications taken to manage their symptoms Amyotrophic lateral sclerosis (ALS): Due to the steady, progressive and irreversible degeneration of upper & lower motor neurons - Involved progressive muscle weakness, leading to respiratory failure & death, usually within 2-5 years of onset - Muscles atrophy as a result of disuses (secondary to the loss of nerve innervation) and as the disease progresses, it eventually reaches the respiratory muscles - Patients become apnoeic (unless ventilated) and this is the reason they may be encountered in the prehospital setting - Can also be called ‘Lou Gherigs disease’, but was also the cause of Stephen Hawking's disability Multiple sclerosis: Steady, progressive & irreversible degeneration of the myelin sheath, primarily in the CNS - MS is the most frequent cause of permanent disability in young adults, aside from trauma, with onset predominantly in the 20-40 year age group - Though the exact cause remains unclear, it is thought to be an autoimmune disorder, and links to the human leukocyte antigen (HLA) complex responsible for numerous immune functions - MS ‘attacks’ or ‘flare ups’ vary widely, ranging from generalised weakness and paralysis to balance issues, to paraesthesia or vision problems Myasthenia Gravis: Chronic autoimmune disorder characterised by the destruction of nicotinic Ach receptors at the postsynaptic neuromuscular junction (destroy the communication between the nerves & the muscles they innervate) - Results in weakness of the voluntary skeletal muscles of the body, especially those controlling the eyes, mouth, & limbs - Symptoms include episodic muscle weakness & easy fatigability, which worsens with activity & decreases with rest - Eye weakness is very common & is often the first sign - Myasthenic crisis occurs when respiratory muscles are affected & hypopnea or apnea occurs Altered mental status differentials: Syncope: 1. Psychogenic syncope - Psychologically shocking or overwhelming stimuli causes (for unknown reasons) bradycardia & peripheral vasodilation, leading to cerebral hypoperfusion 2. Vasovagal syncope - PSNS stimulation (bradycardia & vasodilation) that originates in the baroreceptors of large arteries and produces reflex vagal effects, leading to syncope. - Coughing, neck-tie syndrome & valsalva manoeuvre 3. Gastrogenic syncope - The Vagus nerve innervates the GI tract from mouth to anus. GI stimulation can therefore result in a vagal response. - Gastric or colonic distension, gagging, diarrhoea, esophageal obstruction, abdominal trauma 4. Neurocardiogenic syncope - Prolonged standing promotes pooling of blood in the legs, which is opposed by sympathetic stimulation in order to constrict blood vessels and return blood to the heart. The sympathetic overload increases pressure in the left ventricles, which triggers a ‘slow-down’ reflex (the Bezold-Jarisch reflex) in the heart & lungs, leading to decreased cardiac output and cerebral hypoperfusion, resulting in syncope. 5. Induced vagal response - Carotid sinus massage, Valsalva Maneuver, gagging, cold water facial immersion, rectal stimulation, direct ocular or sinus pressure Syncope: A transient loss of consciousness due to transient global cerebral hypoperfusion characterised by: - Rapid onset - Short duration - Spontaneous complete recovery Cerebral perfusion - CPP = MAP - ICP - In syncope, as ICP is not affected, it is BP that makes the changes, which is controlled by the autonomic nervous system - BP = CO (HR X SV) X SVR Syncope is the symptom, not the disease. Have a high index of suspicion that they will have an systemic illness Syncope is classified by its underlying mechanism: - Neuro-mediated (reflex syncope) - Cardiac - Orthostatic - Unknown Patients can also experience prodromal symptoms known as pre-syncope, including sweating, nausea, lightheadedness & vision alterations Neuro-mediated syncope: Occurs due to overstimulation of the neural reflexes that activate the parasympathetic nervous system. This results in bradycardia, vasodilation and hypotension. - Accounts for 21% of syncope in the general population & 35-47% in EDs. - Affects heart rate & SVR that make up BP - Neural reflexes most commonly result from Vagus nerve stimulation (glossopharyngeal is second most likely). Vagus nerve makes up 75% of nerve fibres from the parasympathetic nervous system - Stimulation can occur in multiple locations in the body from a variety of triggers Neuro-mediated triggers: - Carotid sinus massage (glossopharyngeal nerve) (too tight necktie, accidentally from shaving) - Valsalva manoeuvre / Vasovagal (stimulate vagus nerve in baroreceptors of the heart) - Gagging, vomiting, coughing (increases intrathoracic pressure, activating vagus nerve) - Rectal stimulation (bearing down, also vagus nerve innervated entire GI tract, so bowel movements can trigger this) - Pain & emotional distress (undifferentiated area in the central nervous system) Cardiac syncope: Cardiac syncope is any transient alteration of normal cardiac activity causing syncope. - Affects HR & SV components - Can be due to a rhythm disturbance, or a structural abnormality with impaired cardiac output - Rhythm disturbances:  - Bradycardia (sinus pause, sick sinus syndrome, atrioventricular blocks, Afib) - Tachycardia causing reduced stroke volume (VT, SVT) - Arrhythmias account for 11% of all syncopal episode, increasing with age - Structural abnormalities: - Circulatory demand outweighs the impaired ability of the heart to increase its output (cardiac failure, STEMI, valvular disease, cardiomyopathy, pericarditis, cardiac tamponade, aortic stenosis) - Patients over 65 are 4X more likely to have a cardiac syncope versus non cardiac syncope Orthostatic syncope: Due to orthostatic hypotension (OH), which is defined as an abnormal decrease in systolic blood pressure on standing. - Only involves SVR - Accounts for 9.5% of syncope - Venous return rapidly decreases on standing due to gravity. In OH, the SVR response to this postural change is inadequate, leading to hypotension. - Three types of OH: - Classic OH: SBP drop of >20mmHg, or DBP drop of >10mmHg within 3 minutes of standing - Initial OH: SBP drop of >40mmHg after standing & quickly returns to normal - Delayed OH: A delayed & progressive drop in BP after standing (attributed to the impairment of compensatory mechanisms & stiffer hearts reducing abi\litiy to preload, especially in older populations) - Unlike neuro-mediated syncope, there is no decrease in heart rate, and reflex tachycardia is usually seen. (However, differs from POTS as must have syncope, but tachycardia is optional, whereas POTS must have tachycardia & syncope is optional) Syncope consideration: - Prognosis: consider risk of life threatening event, and risk of recurrence & injury - Every syncope patient should have a 12 lead ECG to look for cardiac cause - Biggest predictor of poor prognosis is advancing age (>40) - Other risk factors: - Comorbidities, any cardiac history, shortness of breath, palpitations, hypotension Postural orthostatic tachycardia syndrome: A form of orthostatic intolerance, characterised by an increase in HR >30 bpm or tachycardia >120 bpm, within 10 minutes of standing, and instability of blood pressure (hypotension) - Affects the HR (tachycardia) - Patients may experience palpitations, lightheadedness, & orthostatic syncope, which can all be relieved by lying down. - POTS affects predominantly females aged 15-50 - Treatment & management can include increasing salt & fluid intake, as well as medications that may increase blood volume, or narrow blood vessels, as well as beta blockers to keep their HR down.