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CNS CONDITIONS Flashcards

1
Q

MULTIPLE SCLEROSIS (MS) - DEFINITION

A
  • MS is an autoimmune disease
  • This is when the immune system mistakenly attacks healthy cells
  • In people with MS the immune system attacks cells in the myelin, which is the protective sheath that surrounds nerves in the brain and spinal cord
  • Damage to the myelin sheath interrupts nerve signals from the brain to other parts of the body
  • The damage can lead to symptoms affecting the brain, spinal cord and eyes
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2
Q

MULTIPLE SCLEROSIS (MS) - TYPES

A
  • 4 types of MS
  • Clinically isolated syndrome (CIS)
    o When someone has a first episode of MS symptoms, it is often categorised as CIS. Not everyone who has CIS goes on to develop MS
  • Relapsing-remitting MS (RRMS)
    o Most common form
    o People with RRMS have flare ups of new or worsening symptoms
    o Periods of remission follow the flare-ups
  • Primary progressive MS (PPMS)
    o Symptoms slowly and gradually worsen without any periods of relapse or remission
  • Secondary progressive MS (SPMS)
    o In many cases people originally diagnosed with RRMS eventually progress to SPMS
    o With this nerve damage is accumulated and symptoms progressively worsen
    o There may still be flare-ups but without the periods of remission after
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3
Q

MULTIPLE SCLEROSIS (MS) - CAUSE

A
  • No definite cause is known
  • Factors that may trigger MS
    o Exposure to certain viruses or bacteria
    o Where you live – areas further from the equator have higher rates of MS
    o How the immune system functions
    o Gene mutations
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4
Q

MULTIPLE SCLEROSIS (MS) - POPULATION AFFECTED

A

Female, white adults aged between 20 and 40

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5
Q

MULTIPLE SCLEROSIS (MS) - RISK FACTORS

A
  • Age – 20 – 40
  • Sex – women are more likely by 2 to 3 times
  • Family history
  • Certain infections
  • Race – white people
  • Climate – cold climate more likely
  • Vitamin D
  • Genes
  • Obesity
  • Certain autoimmune diseases
  • Smoking
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6
Q

MULTIPLE SCLEROSIS (MS) - CLINICAL PRESENTATION

A
  • Signs and symptoms may differ greatly from person and over the course of the disease depending on the location of the affected nerve fibres
  • Numbness or weakness in one or more limbs that typically occurs on one side of the body at a time
  • Tingling
  • Electric-shock sensations that occur with certain neck movements
  • Lack of coordination
  • Unsteady gait or inability to walk
  • Partial or complete loss of vision, usually in one eye at a time, often with pain during eye movement
  • Prolonged double vision
  • Blurry vision
  • Vertigo
  • Problems with sexual, bowel and bladder dysfunction
  • Fatigue
  • Slurred speech
  • Cognitive problems
  • Mood disturbances
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7
Q

MULTIPLE SCLEROSIS (MS) - DIAGNOSIS

A
  • Multiple tests are used to diagnose MS
  • Blood tests
  • MRI
    o MRI looks for evidence of lesions in the brain or spinal cord that indicate MS
  • Lumbar puncture
  • Evoked potentials test
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8
Q

MULTIPLE SCLEROSIS (MS) - TREATMENT

A
  • Currently no cure for MS
  • Treatment focuses on managing symptoms, reducing relapses and slowing the diseases progression
  • DMTs
  • Relapse management medications
    o High dose of corticosteroids for a severe attack
  • Physical rehabilitation
  • Mental health counselling
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9
Q

MULTIPLE SCLEROSIS (MS) - PREVENTION

A
  • Eating a healthy diet
  • Getting regular exercise
  • Managing stress
  • Not smoking and limiting alcohol intake
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10
Q

MULTIPLE SCLEROSIS (MS) - PROGNOSIS

A
  • In some cases, MS does lead to disability and loss of some physical or mental function
  • Most people with MS will continue to lead full, active and productive lives
  • Taking steps to manage health and lifestyle can help improve the long-term outcome
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11
Q

AMYOTROPHIC LATERAL SCLEROSIS (ALS) - DEFINITION

A
  • ALS is a type of motor neuron disease
  • It is also known as Lou Gehrig’s disease
  • ALS affects motor neurons – nerves that control the voluntary muscles
  • Voluntary muscles are the ones used for actions like chewing, talking and moving the arms and legs
  • It is a neuromuscular disorder that causes muscle weakness
  • It affects both the upper and lower motor neurons
  • In ALS the muscles begin to atrophy, making it difficult to walk, talk, swallow and eventually breathe
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12
Q

AMYOTROPHIC LATERAL SCLEROSIS (ALS) - TYPES OF ALS

A
  • Classical ALS
    o Most common type, affects more than 2/3 of people with ALS
    o Both the upper and lower motor neurons decline
  • Progressive bulbar palsy (PBP)
    o Affects about 25% of people with ALS
    o It starts with difficulty speaking, chewing and swallowing caused by a breakdown of the upper and lower motor neurons to the mouth and throat
    o This will sometimes worsen to affect the rest of the body, in which case the condition is called bulbar-onset ALS
  • Progressive muscular atrophy (PMA)
    o Affects only the lower motor neurons
  • Primary lateral sclerosis
    o Rarest form of ALS
    o Only the upper motor neurons decline
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13
Q

AMYOTROPHIC LATERAL SCLEROSIS (ALS) - CATEGORIES OF ALS

A
  • Sporadic ALS
    o About 90% to 95% of ALS cases are sporadic
    o The disease happens randomly
    o It is not tied to any clear factor or family history of the disease
  • Familial ALS
    o Affects 5% to 10% of people with ALS
    o It happens when you inherit the disease from one or both of your parents
    o The disease runs in families and gets passed down through genetic mutations or changes
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14
Q

AMYOTROPHIC LATERAL SCLEROSIS (ALS) - CAUSE

A
  • Its not known what causes ALS
  • It is believed to be a combo of factors
  • Genetics
    o Mutations or changes in certain genes may lead to motor neuron breakdown
  • Environment
    o Getting exposed to certain toxic substances, viruses or physical trauma may cause ALS
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15
Q

AMYOTROPHIC LATERAL SCLEROSIS (ALS) - POPULATION AFFECTED

A

White men aged between 55 and 75

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16
Q

AMYOTROPHIC LATERAL SCLEROSIS (ALS) - RISK FACTORS

A
  • Age – between 55 and 75
  • Race and ethnicity – white people and non-Hispanics
  • Sex – earlier in life, men are at a higher risk than men but as age increases, the risk is about the same
  • Military veterans
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17
Q

AMYOTROPHIC LATERAL SCLEROSIS (ALS) - CLINICAL PRESENTATION

A
  • At first, you may notice muscle weakness or stiffness
  • Limb onset ALS is when the symptoms start in the legs or arms
  • Bulbar onset is when the symptoms start with your speech or swallowing
  • No matter where the ALS symptoms begin, they soon spread to other parts of the body
  • Initial symptoms include
    o Muscle cramps and twitching, especially in the hands and feet
    o Fasciculations
    o Difficulty using arms and legs
    o Thick speech and difficulty projecting the voice
    o Weakness and fatigue
    o Weight loss
  • As ALS gets more severe symptoms include
    o Shortness of breath
    o Difficulty breathing, chewing and swallowing
    o Inability to stand or walk independently
    o Weight loss, since people with ALS burn calories at a faster rate
    o Depression and anxiety as people become aware of what is happening to them
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18
Q

AMYOTROPHIC LATERAL SCLEROSIS (ALS) - CLINICAL PRESENTATION - BREATHING PROBLEMS

A

o Shortness of breath, even during rest
o Weak cough
o Difficulty clearing throat or lungs
o Extra saliva
o Inability to lie flat in bed
o Repeated chest infections and pneumonia
o Respiratory failure

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19
Q

AMYOTROPHIC LATERAL SCLEROSIS (ALS) - DIAGNOSIS

A
  • Blood test
  • Urine test
  • A neurological examination – to test reflexes
  • Electromyogram (EMG)
  • A nerve conduction study
  • MRI
  • Other tests cant diagnose ALS but can rule out other diseases
    o A spinal fluid test
    o A muscle and/or nerve biopsy
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20
Q

AMYOTROPHIC LATERAL SCLEROSIS (ALS) - TREATMENT

A
  • No cure
  • Treatment can slow progression of the disease
  • Medications
    o To relieve muscle cramps, extra saliva and other symptoms
    o Riluzole – may help reduce damage to the motor neurons, it cannot reverse damage that has already occurred
    o Edaravone – can slow the decline in someone’s functioning
  • Physical therapy – to stay mobile
  • Nutritional counselling
  • Speech therapy
  • Assistive devices
  • Special equipment
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21
Q

AMYOTROPHIC LATERAL SCLEROSIS (ALS) - PREVENTION

A
  • No proven way to prevent ALS
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22
Q

AMYOTROPHIC LATERAL SCLEROSIS (ALS) - PROGNOSIS

A
  • A persons prognosis depends on how quickly the symptoms progress
  • People with ALS typically live for 3 to 5 years after diagnosis
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23
Q

EPILEPSY - DEFINITION

A
  • Epilepsy is a chronic disease that causes repeated seizures due to abnormal electrical signals produced by damaged brain cells
  • A burst of uncontrolled electrical activity within brain cells causes a seizure
  • Seizures can include changes to the patients awareness, muscle control, sensations, emotions and behaviour
  • Epilepsy is also called a seizure disorder
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24
Q

EPILEPSY - CAUSE

A
  • In up to 70% of cases the cause of seizures is unknown
  • Known causes include
    o Genetics
    o Mesial temporal sclerosis
    o Head injuries
    o Brain infections
     Meningitis
     Encephalitis
    o Immune disorders
    o Developmental disorders
     Focal cortical dysplasia
     Polymicrogyria
     Tuberous sclerosis
    o Metabolic disorders
    o Brain conditions and brain vessel abnormalities
     Brain tumours
     Strokes
     Dementia
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25
Q

EPILEPSY - POPULATION AFFECTED

A

Anyone, at any age, race or sex

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26
Q

EPILEPSY - FOCAL ONSET SEIZURES - FOCAL ONSET AWARE SEIZURE

A

 Pt is awake and aware during the seizure
 Changes in the senses – how things taste, smell or sound
 Changes in emotions
 Uncontrolled muscle jerking, usually in arms or legs
 Seeing flashing lights, feeling dizzy, having tingling sensation

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27
Q

EPILEPSY - FOCAL ONSET SEIZURES - FOCAL ONSET IMPAIRED AWARENESS SEIZURE

A

 Pt is confused or have lost awareness or consciousness during the seizure
 Blank stare or a ‘staring into space’
 Repetitive movements like eye blinking, lip-smacking or chewing motion, hand rubbing or finger motions

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28
Q

EPILEPSY - GENERALISED ONSET SEIZURES - ABSENCE SEIZURES

A

 Causes a blank stare
 There may be minor muscle movements, including eye blinking, lip-smacking or chewing motions, hand motions or rubbing fingers
 More common in children
 Last for only a few seconds
 Commonly mistaken for daydreaming

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29
Q

EPILEPSY - GENERALISED ONSET SEIZURES - ATONIC SEIZURES

A

 Atonic means without tone
 Lose of muscle control or the muscles are weak during the seizure
 Parts of the body may droop or drop such as eyelids or head
 Pt may fall to the ground during this short seizure
 Sometimes called a drop attack or drop seizure

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30
Q

EPILEPSY - GENERALISED ONSET SEIZURES - TONIC SEIZURES

A

 Tonic means with tone
 Means muscle tone is increased during the seizure
 Arms, legs, back or whole body may be tense or stiff causing the pt to fall
 You may be aware or have a small change in awareness during this short seizure

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31
Q

EPILEPSY - GENERALISED ONSET SEIZURES - CLONIC SEIZURES

A

 Clonus means fast, repeating stiffening and relaxing of a muscle
 Happens when muscles continuously jerk for seconds to a minute or muscles stiffen followed by jerking for seconds up to 2 minutes

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32
Q

EPILEPSY - GENERALISED ONSET SEIZURES - TONIC-CLONIC SEIZURES

A

 Combo of muscle stiffness (tonic) and repeated rhythmic muscle jerking (clonic)
 Pt will lose consciousness, fall to the ground, muscles stiffen and jerk for 1 to 5 minutes
 Pt may bite their tongue, drool, lose muscle control of bladder or bowels

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33
Q

EPILEPSY - GENERALISED ONSET SEIZURES - MYOCLONIC SEIZURES

A

 Seizure type causes brief, shock-like muscle jerks or twitches
 Usually last only a couple of seconds

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34
Q

EPILEPSY - RISK FACTORS

A
  • Brain infections
  • Seizures in childhood
  • Dementia
  • Stroke and other vascular diseases
  • Head injuries
  • Family history
  • Age – onset is most common in children and older adults
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35
Q

EPILEPSY - CLINICAL PRESENTATION

A
  • Main symptom of epilepsy is recurring seizures
  • Symptoms vary depending on the type of seizure
  • Temporary loss of awareness of consciousness
  • Uncontrolled muscle movements
    o Muscle jerking
    o Loss of muscle tone
  • Blank stare or staring into space look
  • Temporary confusion, slowed thinking, problems with talking and understanding
  • Changes in hearing, vision, taste, smell, feelings of numbness or tingling
  • Problems talking or understanding
  • Upset stomach
  • Waves of heat or cold, goosebumps
  • Lip-smacking, chewing motion, rubbing hands, finger motions
  • Psychic symptoms
    o Fear
    o Dread
    o Anxiety
    o Déjà vu
  • Faster heart rate and/or breathing
  • Most people with epilepsy tend to have the same type of seizure so similar symptoms with each seizure
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36
Q

EPILEPSY - SYMPTOMS OF A SEIZURE

A
  • Muscle jerks
  • Muscle stiffness
  • Loss of bowel or bladder control
  • Change in breathing
  • Skin colour turned pale
  • Had a blank stare
  • Lost consciousness
  • Had problems talking or understanding what was said to you
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37
Q

EPILEPSY - DIAGNOSIS

A
  • Technically, if the pt experiences 2 or more seizures that weren’t caused by a known medical condition, they are considered to have epilepsy
  • EEG
  • Brain scan – MRI
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38
Q

EPILEPSY - TREATMENT

A
  • Anti-seizure medications
    o Is appropriate treatment for up to 70% of patients
    o Choice of anti-seizure medication depends on
     Seizure type
     Your prior response to anti-seizure medications
     Other medical conditions you have
     The potential for interaction with other medications you take
     Side effects of the anti-seizure drug
     Age
     General health
     Cost
  • Diet therapy
    o Diets high in fat, moderate in protein and low in carbohydrates
    o Ketogenic diet
    o Modified Atkins diet
  • Surgery and devices
    o Epilepsy surgery can be a safe and effective treatment option when more than 2 anti-seizure medication trials fail to control seizures
    o Surgical resection (removal of abnormal tissue)
    o Disconnection (cutting fibre bundles that connect areas of the brain)
    o Stereotactic radiosurgery (targeted destruction of abnormal brain tissue)
    o Implantation of neuromodulation devices
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39
Q

EPILEPSY - PREVENTION

A
  • Many cases are out of the patients control and cannot be prevented
  • You can reduce the chances of developing a few conditions that might lead to epilepsy
    o Lower the risk of a traumatic brain injury by wearing your seatbelt and wearing a bike helmet
    o Lower the risk of stroke by eating a healthy diet, maintaining a healthy weight and exercising regularly
    o Seek therapy for substance abuse
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40
Q

EPILEPSY - PROGNOSIS

A
  • No cure
  • Many options to treat
  • About 70% of people become seizure-free with proper treatment within a few years
    o The remaining 30% are considered to have drug-resistant epilepsy and can be considered for epilepsy surgery
  • Some people will require life-long medication
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41
Q

PAIN PHYSIOLOGY - HOW DO WE FEEL PAIN?

A
  • There are special nerve cell endings that initiate the sensation of pain
  • These nerve cells ae known as nociceptors
  • The CNS is very important in pain registration
  • The spinal cord is like a relay station where the info about pain, temperature, pressure from the periphery can travel up to the brain
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42
Q

PAIN PHYSIOLOGY - WHAT ARE THE BARRIERS OF THE SPINAL CORD?

A

o Pia mater
o Arachnoid
o Dura mater
o These are collectively known as the meninges

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43
Q

PAIN PHYSIOLOGY - WHAT ARE THE BARRIERS OF THE SPINAL CORD?

A

o Pia mater
o Arachnoid
o Dura mater
o These are collectively known as the meninges

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44
Q

PAIN PHYSIOLOGY - WHAT WILL A CROSS SECTION OF THE SPINAL CORD SHOW?

A

o White matter
 White matter contains the axons of the nerve cells
o Grey matter (usually butterfly shaped and is inside the white matter)
 Grey matter contains the cell bodies of the nerve cells itself
o Central canal
 Central canal contains cerebrospinal fluid – this is an important fluid for nourishing the CNS

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45
Q

PAIN PHYSIOLOGY - NOCICEPTORS

A
  • Nociceptors are the pain sensing nerve cells
    o Alpha-delta fibres
     Very small myelinated nerve cells
     Produce fast, well localised sharp pain
    o C fibres
     Unmyelinated
     Produce slow, poorly localised pain
     These produce the burning, throbbing type pain
  • Nociceptors can also be referred to as the afferent nerve fibres because it is bringing info into the spinal cord to the second order neuron
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46
Q

PAIN PHYSIOLOGY - ACTIVATION OF PAIN SIGNALS

A
  • Pain receptors, called nociceptors, are specialised nerve endings that detect noxious (harmful) stimuli such as heat, pressure, or chemicals
  • When these receptors are activated, they send electrical signals to the spinal cord
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47
Q

PAIN PHYSIOLOGY - TRANSMISSION OF PAIN SIGNALS

A
  • The signals from the pain receptors travel through the nerves to the spinal cord and then to the brain
  • Along the way, they are modulated by various neurotransmitters and other substances that can enhance or inhibit the pain signals
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48
Q

PAIN PHYSIOLOGY - PROCESSING OF PAIN SIGNALS IN THE BRAIN

A
  • The brain processes the incoming pain signals and interprets them as pain
  • The somatosensory cortex is responsible for the perception of pain and the location of the pain sensation in the body
  • The limbic system, which is involved in emotion and memory, can also modulate the pain experience and contribute to the emotional aspect of pain
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49
Q

PAIN PHYSIOLOGY - PAIN RESPONSE

A
  • The perception of pain triggers a response in the body, such as a reflexive withdrawal from a noxious stimulus or the release of stress hormones
  • The response to pain can also be modulated by various factors, such as previous experiences with pain, expectations and cultural influences
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50
Q

PAIN PHYSIOLOGY - CHRONIC PAIN

A
  • Chronic pain is pain that persists for longer than 3 months
  • Chronic pain can involve changes in the nervous system that result in increased sensitivity to pain signals and a heightened pain response
  • This can lead to a cycle of pain and stress that can be difficult to break
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51
Q

PAIN PHYSIOLOGY - SOMATOSENSORY CORTEX

A
  • The somatosensory cortex is a region of the brain that is responsible for processing info related to touch, proprioception and pain sensations
  • It is located in the parietal lobe of the brain and is organised into different regions or ‘maps’ that correspond to different parts of the body
  • When you touch or feel something, sensory info is transmitted from the PNS to the somatosensory cortex, which processes and interprets the info
  • The somatosensory cortex is essential for the sense of touch and it also plays a role in the body awareness and movement control
  • Dysfunction or damage to this area of the brain can lead to various sensory disorders, such as numbness, tingling or loss of sensation
  • Homunculus – the primary somatosensory cortex
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52
Q

PAIN PHYSIOLOGY - THE HOMUNCULUS

A
  • The homunculus is also known as the sensory or motor homunculus
  • It is a visual representation of the human body that is mapped onto the somatosensory cortex and motor cortex in the brain
  • It is a distorted representation of the body, where body parts that are more sensitive or have more motor control are represented by larger areas of the cortex
  • The somatosensory homunculus maps the body’s sensory receptors onto the somatosensory cortex, whth areas that are more sensitive having larger representations
    o E.g. the lips and fingertips have a larger representation compared to the torso or limbs
  • This is because these areas have a higher density of sensory receptors and require more precise discrimination
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53
Q

PAIN PHYSIOLOGY - THE ASCENDING PATHWAYS

A
  • The ascending pathway in pain physiology refers to the pathway that carries pain signals from the periphery of the body (such as skin, muscles and organs) up to the brain for processing and perception
  • The process of pain transmission starts when nociceptors are activated by noxious stimuli, such as mechanical, thermal or chemical damage
  • The activation of nociceptors triggers the release of neurotransmitters, such as substance P and glutamate, which propagate the pain signal along the sensory nerve fibres
    o The sensory nerve fibres are also known as primary afferent fibres
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54
Q

PAIN PHYSIOLOGY - PRIMARY AFFERENT NERVE FIBRES

A
  • These primary afferent fibres can be categorised into 2 types based on their diameter and myelination
    o A-delta fibres
    o C fibres
  • A-delta fibres are larger and myelinated, they transmit sharp and well localised pain signals
  • C fibres are smaller and unmyelinated and they transmit dull and diffuse pain signals
  • The primary afferent fibres then synapse with second order neurons in the dorsal horn of the spinal cord
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55
Q

PAIN PHYSIOLOGY - 3 MAIN PATHWAYS THAT THE SECOND ORDER NEURONS USE TO ASCEND TO THE BRAIN

A
  • These second order neurons cross over to the opposite side of the spinal cord before ascending to the brain via the 3 main pathways
    o Spinothalamic tract
    o Spinoreticular tract
    o Dorsal column pathway
  • The spinothalamic tract carries info about the location and intensity of pain to the thalamus, which is a relay station in the brain that directs sensory info to the appropriate cortical areas for further processing
  • The spinoreticular tract carries info about the emotional and autonomic aspects of pain to the reticular formation in the brainstem, which is involved in the regulation of arousal and attention
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56
Q

PAIN PHYSIOLOGY - THE DORSAL COLUMN

A
  • The dorsal column pathway carries info about proprioception, touch and vibration to the brain
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57
Q

PAIN PHYSIOLOGY - WHICH REGIONS OF THE BRAIN PROCESS PAIN?

A
  • Once the pain signals reach the brain, they are processed by various regions
    o The somatosensory cortex
    o The insula
    o The anterior cingulate cortex
    o The prefrontal cortex
  • These are all involved in the perception, localisation and the interpretation of pain
  • Also, the limbic system, which is responsible for emotions and memory, can also modulate the pain experience by amplifying or reducing the pain signals
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58
Q

PAIN PHYSIOLOGY - THE DESCENDING PATHWAY

A
  • The descending pathway in pain physiology refers to the pathway that originates in the brain and modulates the transmission of pain signals in the spinal cord
  • The descending pathway is a complex network of neurons that originates in various regions of the brain
    o The periaqueductal gray (PAG)
    o The rostral ventromedial medulla (RVM)
    o The dorsolateral prefrontal cortex (DLPFC)
  • These regions of the brain play a crucial role in the modulation of pain by releasing neurotransmitters
    o Endorphina
    o Enkephalins
    o Dynorphins
  • The descending pathway is not only involved in pain modulation but also plays a role in the regulation of other physiological processes, such as mood, stress and immune function
  • Dysfunction in the descending pathway can lead to chronic pain syndromes
    o Fibromyalgia
    o Neuropathic pain
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59
Q

PAIN PHYSIOLOGY - 2 MAIN SYSTEMS OF THE DESCENDING PATHWAY

A
  • The descending pathway can be divided into 2 main systems
    o The opioid system
    o The non-opioid system
  • The opioid system involves the release of endogenous opioids, such as endorphins and enkephalins, which bind to opioid receptors located on pain-sensing neurons in the spinal cord
  • This inhibits the release of neurotransmitters and reduces the transmission of pain signals to the brain
  • The non-opioid system involves the release of other neurotransmitters, such as serotonin and norepinephrine, which act on receptors located on pain-sensing neurons and also inhibit pain transmission
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60
Q

PAIN PHYSIOLOGY - 2 MAIN PATHWAYS OF THE DESCENDING PATHWAY

A
  • The descending pathway can also be further divided into 2 pathways
    o The direct pathway
    o The indirect pathway
  • The direct pathway involves the activation of inhibitory neurons in the spinal cord by the descending neurons, which directly inhibit the transmission of pain signals
  • The indirect pathway involves the activation of excitatory neurons in the spinal cord, which release neurotransmitters that inhibit inhibitory neurons, thereby increasing the transmission of pain signals
  • The balance between the direct and indirect pathways is important in determining the level of pain perception
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61
Q

PAIN PHYSIOLOGY - SUBSTANTIA GELATINOSA

A
  • The substantia gelatinosa (SG) is a specialised layer of grey matter located in the dorsal horn of the spinal cord
  • It plays a critical role in the processing and modulation of pain signals
  • The SG contains a complex network of interneurons that receive inputs from the primary afferent fibres that transmit pain signals from the periphery of the body
  • The interneurons are classified into different subtypes based on their location, morphology and neurotransmitter content
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62
Q

PAIN PHYSIOLOGY - FUNCTIONS OF THE SUBSTANTIA GELATINOSA INTERNEURONS

A
  • The SG interneurons are involved in a variety of functions, including
    o The modulation of pain signals
    o The integration of sensory info
    o The coordination of motor responses
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63
Q

PAIN PHYSIOLOGY - SUBSTANTIA GELATINOSA AND THE MODULATION OF PAIN SIGNALS

A
  • One of the most important functions of the SG is the modulation of pain signals
  • The SG receives inputs from both A-delta and C fibres that transmit pain signals
  • The SG also contains specialised interneurons that release neurotransmitters, such as enkephalin, which can inhibit the transmission of pain signals
  • This process is known as presynaptic inhibition and it occurs when the enkephalin released by the SG interneurons binds to the presynaptic terminals of the primary afferent fibres, inhibiting the release of neurotransmitters that transmit pain signals
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64
Q

PAIN PHYSIOLOGY - SUBSTANTIA GELATINOSA AND THE INTEGRATION OF SENSORY INFORMATION

A
  • Another important function of the SG is the integration of sensory info
  • The SG receives inputs from different types of sensory neurons, including those that transmit info about touch, pressure, temperature and vibration
  • The SG interneurons integrate these different types of sensory info and relay them to higher centres in the brain for further processing
  • The SG also plays a role in coordination and motor responses
  • This means that the SG interneurons can modulate the activity of motor neurons and coordinate muscle responses for things such as the withdrawal reflex
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65
Q

BACTERIAL MENINGITIS - DEFINITION

A
  • Acute bacterial meningitis is the most common form of meningitis
  • The infection can cause the tissues around the brain to swell
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66
Q

BACTERIAL MENINGITIS - CAUSE

A
  • The bacteria most often responsible for bacterial meningitis are common in the environment and can also be found in the nose and respiratory system without causing any harm
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67
Q

BACTERIAL MENINGITIS - POPULATION AFFECTED

A
  • Children between 1 month and 2 years are most susceptible
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68
Q

BACTERIAL MENINGITIS - RISK FACTORS

A
  • Alcohol abuse
  • Have chronic nose or ear infections
  • Sustain a head injury
  • Get pneumococcal pneumonia
  • Weakened immune system
  • Brain or spinal surgery
  • Have a widespread blood infection
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69
Q

BACTERIAL MENINGITIS - CLINICAL PRESENTATION

A
  • High fever, Headaches
  • An inability to lower the chin to the chest due to stiffness in the neck
  • Confusion, Irritability
  • Seizures and stroke may occur
  • In young children
    • Fever may cause vomiting
    • Refusal to eat
    • Very irritable and crying
    • May be seizures
    • Swelling of the head (less common)
  • Onset of symptoms is fast, within 24 hours
  • Physical exam
    • Look for a purple or red non-blanching rash
    • Check neck stiffness
    • Exam hip and knee flexion
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70
Q

BACTERIAL MENINGITIS - PROGNOSIS

A
  • 10% death rate from bacterial meningitis
  • Most people recover if diagnosed and treated early
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71
Q

VIRAL MENINGITIS - DEFINITION

A
  • Infection and inflammation of the fluid membranes surrounding the brain and spinal cord
  • These membranes are called meninges
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72
Q

VIRAL MENINGITIS - CAUSE

A
  • Most cases are due to a group of viruses called enteroviruses
  • Most common in late summer and early fall
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73
Q

VIRAL MENINGITIS - POPULATION AFFECTED

A
  • Children under 5
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74
Q

VIRAL MENINGITIS - RISK FACTORS

A
  • Skipping vaccinations
  • Age- under 5
  • Living in a community setting
  • Pregnancy
  • Weakened immune system
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75
Q

VIRAL MENINGITIS - CLINICAL PRESENTATION - OVER 2 YEARS

A
  • Sudden high fever
  • Stiff neck
  • Severe headache
  • Nausea or vomiting
  • Confusion
  • Trouble concentrating
  • Seizures
  • Sleepiness or trouble waking
  • Sensitivity to light
  • No appetite or thirst
  • Skin rash in some cases, such as in meningococcal meningitis
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76
Q

VIRAL MENINGITIS - CLINICAL PRESENTATION - NEW-BORNS

A
  • Nigh fever
  • Constant crying
  • Being very sleepy or irritable
  • Trouble waking from sleep
  • Being inactive or sluggish
  • Not waking to eat
  • Poor feeding
  • Vomiting
  • A bulge in the soft spot on top of the baby’s head
  • Stiffness in the body and neck
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77
Q

VIRAL MENINGITIS - PROGNOSIS

A
  • Viral meningitis can go away on its own within about a week
  • Will probably need treatment
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78
Q

MOTORNEURONE DISEASE - DEFINITION

A
  • Motor neurone disease (MND) is an uncommon condition that affects the brain and nerves
  • It causes weakness
  • It is a progressive disease and gets worse over time
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79
Q

MOTOTNEURONE DISEASE - CAUSE

A
  • MND occurs when specialist nerve cells (motor neurones) in the brain and spinal cord progressively fail
  • Genetic causes
    • 20% of cases linked to genetic causes
    • Family history is an important factor
80
Q

MOTORNEURONE DISEASE - POPULATION AFFECTED

A
  • Mostly affects people in their 60s and 70s
81
Q

MOTORNEURONE DISEASE - RISK FACTORS

A
  • Genetics
  • Family history of frontotemporal dementia
  • Exposure to viruses
  • Exposure to certain toxins and chemicals
  • Inflammation and damage to neurons caused by an immune system response
  • Nerve growth factors
  • Growth, repair and ageing of motor neurons
82
Q

MOTORNEURONE DISEASE - CLINICAL PRESENTATION

A
  • Muscle aches, cramps and twitching
  • Clumsiness and stumbling
  • Weakness or changes in hands, arms, legs and voice
  • Slurred speech, swallowing or chewing difficulty
  • Fatigue
  • Muscle wasting
  • Weight loss
  • Emotional lability
  • Cognitive change
  • Respiratory changes
  • Effects of MND
    • Develop generalised paralysis
    • Lose speech and have difficulty swallowing
    • Become breathless and experience sleep disturbances
    • Experience mild cognitive and behavioural change
    • Become increasingly dependent on others for all aspects of day-to-day activity
83
Q

PARKINSON’S DISEASE - DEFINITION

A
  • A progressive disorder that affects the nervous system and the parts of the body controlled by the nerves
84
Q

PARKINSON’S DISEASE - CAUSE

A
  • Certain nerve cells (neurons) in the brain gradually break down or die
  • Many of the symptoms are due to a loss of neurons that produce a chemical messenger in your brain – dopamine
  • When dopamine levels decrease, it causes atypical brain activity, leading to impaired movement and other symptoms of Parkinson’s disease
  • Exact cause is unknown but several factors appear to play a role
    • Genes
    • Environmental triggers
      • Certain toxins or environmental factors
85
Q

PARKINSON’S DISEASE - POPULATION AFFECTED

A
  • Menat middle to late age
86
Q

PARKINSON’S DISEASE - RISK FACTORS

A
  • Age - Ordinarily begins in middle or later life, Risk increases with age, Usually developed around 60 or later
  • Heredity - Having a close relative with the disease increases the chances that you will also develop it
  • Sex - Men more likely
  • Exposure to toxins - Ongoing exposure to herbicides and pesticides may slightly increase the risk
87
Q

PARKINSON’S DISEASE - CLINICAL PRESENTATION

A
  • S&S can be different for everyone
  • Early signs may be mild and go unnoticed
  • Symptoms often begin on one side of the body and usually remain worse on that side
  • Tremor - Rhythmic shaking, Usually begins in a limb, often in hand or fingers, Hand may tremor at rest, Tremor may decrease when patient is performing tasks
  • Bradykinesia - Slowed movement, Happens overtime, Can make simple tasks difficult and time consuming, Steps may become shorter, May become more difficult to get out of a chair
  • Rigid muscles - Stiff muscles can be painful, May limit ROM
  • Impaired posture and balance - Posture may become stooped, May fall or have balance issues
  • Loss of automatic movements
    • Decreased ability to perform unconscious movements - Blinking, Smiling, Swinging arms when walking
    • Speech changes - May speak softly, quickly, slur or hesitate before talking, Speech may become more monotone
    • Writing changes - Harder to write, Writing may appear small
88
Q

TEMPORAL ARTERITIS - DEFINITION

A
  • Inflammation of lining of arteries
  • Aka giant cell arteritis
89
Q

TEMPORAL ARTERITIS - CAUSE

A
  • Caused by inflammation of blood vessels
  • This narrows blood vessels reducing amount of blood and oxygen to reach body tissue
  • Almost any artery can be affected, most common in temples
90
Q

TEMPORAL ARTERITIS - POPULATION AFFECTED

A
  • White women over 70
91
Q

TEMPORAL ARTERITIS - RISK FACTORS

A
  • 70-80
  • Women 2x more likely
  • White people
  • Having PMR
  • Family Hx
92
Q

TEMPORAL ARTERITIS - CLINICAL PRESENTATION

A
  • Head pain and tenderness
  • Scalp tenderness
  • Jaw pain when chewing or opening mouth wide
  • Fever
  • Fatigue
  • Vision loss/double vision
  • Sudden permanent loss of vision
93
Q

SUBARACHNOID HAEMORRHAGE - DEFINITION

A
  • Bleeding between space in brain and surrounding membrane (subarachnoid space)
94
Q

SUBARACHNOID HAEMORRHAGE - CAUSE

A
  • Usually happens when aneurysm bursts in brain
  • Can be caused by trauma, tangle of blood vessels in brain or other health problems
95
Q

SUBARACHNOID HAEMORRHAGE - POPULATION AFFECTED

A
  • Most common in people aged between 45-70
96
Q

SUBARACHNOID HAEMORRHAGE - RISK FACTORS

A
  • Smoking
  • Excessive alcohol consumption
  • High blood pressure
97
Q

SUBARACHNOID HAEMORRHAGE - CLINICAL PRESENTATION

A
  • Described as worst headache ever felt
  • Nausea
  • Vomiting
  • Stiff neck
  • Problems with vision
  • Brief loss of consciousness
98
Q

CRANIAL NERVE DISORDERS - DEFINITION

A
  • The cranial nerves are 12 pairs of nerves that emerge from the brain and are responsible for providing motor and sensory functions
  • Cranial nerve disorder refers to impairment of one of the 12 cranial nerves that emerge from the underside of the brain, pass through openings in the skull, and lead to parts of the head, neck and trunk
99
Q

CRANIAL NERVE DISORDERS - TYPES

A
  • Trigeminal neuralgia
    • Disorder of the 5cranial nerveth
    • Sudden, severe, shock like symptoms across the face
  • Hemifacial spasm
    • Where the blood vessels constrict the 7cranial nerveth
    • Frequent involuntary twitching of the face
  • Glossopharyngeal neuralgia
    • Compression of the 9cranial nerveth
    • Sharp, jabbing px deep in the throat
  • Base skull tumours
    • Can affect any nerve
  • Geniculate neuralgia
    • Deep ear px
  • Occipital neuralgia
    • Distinct type of headache
    • Characterised by sudden and recurring jabs of piercing, throbbing, chronic px
100
Q

CRANIAL NERVE DISORDERS - S&S

A
  • Specific S&S depend on the cranial nerve that is affected
  • Intermittent attacks of excruciating facial px
  • Vertigo
  • Hearing loss
  • Weakness
  • Paralysis
  • Facial twitch
101
Q

DISORDERS AFFECTING THE OLFACTORY NERVE - DEFINITION

A
  • The olfactory nerve is the first cranial nerve (CN I)
  • It is part of the autonomic nervous system, which regulates body functions
  • Nerve enables sense of smell
  • CN I is the shortest sensory nerve in your body – it starts in the brain and ends in the upper, inside part of the nose
102
Q

DISORDERS AFFECTING THE OLFACTORY NERVE - S&S

A
  • Ansomia
    • Complete loss of smell
  • Dysomia
    • Also called phantosmia
    • Unpleasant or strange odours that occur spontaneously
  • Hyposmia
    • Partial loss of smell
  • Parosmia
    • Distorted sense of smell
    • Eg. familiar foods that may smell like chemicals or mold
103
Q

DISORDERS AFFECTING THE OLFACTORY NERVE - CONDITIONS

A
  • Sinus infection
  • Nasal polyps
  • Tobacco use
  • Poor dental hygiene
  • Environmental toxins and chemicals like insecticides
  • Severe head injuries, including concussions
  • Medications like antibiotics
  • Covid
  • Head and neck cancer
  • Diabetes
  • Alzheimer’s disease
  • Brain tumour
  • Parkinson’s disease
  • Epilepsy
104
Q

OCULOMOTOR NERVE PALSY - DEFINITION

A
  • The oculomotor nerve is the 3of 12 cranial nerves (CN III)
  • It is part of the autonomic nervous system
  • It allows movement of the eye muscles, constriction of the pupil, focusing the eyes and the position of the upper eyelid
105
Q

OCULOMOTOR NERVE PALSY - FUNCTION

A
  • Controls 4 of the 6 muscles that enable eye movement
    1. Elevate the upper eyelid
    2. Focus the eyes
    3. Respond to light by making the pupil smaller
    4. Move your eyes inward, outward, up and down and control torsion
106
Q

OCULOMOTOR NERVE PALSY - CAUSE

A
  • Oculomotor palsy is a group of disorders affecting the CN III
  • They occur when the third cranial nerve becomes paralyzed
  • Can be present at birth
  • May occur later in life due to
    • Inadequate blood flow – causes a lack of oxygen that nerves need to function properly
    • Nerve compression – abnormal pressure on a nerve
  • Conditions that may cause oculomotor palsy include
    • Brain aneurysm
    • Brain tumour
    • Head injuries
    • Demyelinating disease - Multiple sclerosis
    • Microvascular disease - Diabetes, High blood pressure
    • Infections - HIV, Lyme disease
    • Migraine
107
Q

TROCHLEAR NERVE PALSY - DEFINITION

A
  • The trochlear nerve is the 4of 12 cranial nerves (CN IV)
  • It is part of the autonomic nervous system
  • It innervates many of the organs, including the eyes
  • It is a motor nerve that sends signals from the brain to the muscles
  • CN IV works with the oculomotor nerve and other eye muscles to control eye movement
108
Q

TROCHLEAR NERVE PALSY - CAUSE

A
  • When the trochlear nerve doesn’t function as it should, its often due to 4nerve palsy – trochlear nerve palsy
  • A palsy occurs when illness or injury paralyzes nerves that control muscle movements
  • In some people its congenital
    • They are born with it
  • It may also be due to trauma from rapid head movements
    • Motor vehicle accidents
  • The trochlear nerve is one of the more fragile cranial nerves because its long and thin
  • Sometimes occurs after minor injuries
  • Less common causes include
    • Cavernous sinus syndrome
      • When an abnormal growth affects the trochlear nerve
    • Guillain-Barre syndrome
    • Lyme disease
    • Meningioma
    • Microvascular coronary disease (MCD)
    • Shingles (herpes zoster)
    • Superior oblique myokymia
      • Episodes of involuntary superior oblique muscle tightening that distorts vision
109
Q

TROCHLEAR NERVE PALSY - TREATMENT

A
  • Treatment depends on what is causing symptoms
  • Vision injuries causes by minor injuries often go away on their own
  • For more severe palsy, treatments may include
    • Eye patch to help the eye rest
    • Special glasses to correct double vision
    • Surgery to repair cranial nerve 4
110
Q

TRIGEMINAL NEURALGIA - DEFINITION

A
  • Causes painful sensations like an electric shock on side of face
  • Chronic pain affects trigeminal nerve, which carries sensations from face to brain
111
Q

TRIGEMINAL NEURALGIA - CAUSE

A
  • Trigeminal nerve function disrupted
  • Contact between blood vessel and nerve at base of brain
  • Contact puts pressure on nerve and causes it to malfunction
112
Q

TRIGEMINAL NEURALGIA - POPULATION AFFECTED

A
  • 50+
  • More common in women than men
113
Q

TRIGEMINAL NEURALGIA - RISK FACTORS

A
  • Hypertension
  • Arteriosclerotic changes
  • Aging
  • Family Hx
114
Q

TRIGEMINAL NEURALGIA - CLINICAL PRESENTATION

A
  • Episodes of severe, shotting or jabbing P that may feel like and electric shock
  • Spontaneous attacks triggered by things such as touching your face
  • Attacks of P lasting a few seconds to several mins
  • P occurs with facial spasms
  • P in areas supplied by trigeminal- jaw, cheek, teeth, gums, lips or forehead
  • P rarely occurs at night while sleeping
115
Q

ABDUCENS NERVE PALSY - DEFINITION

A
  • Most common ocular motor paralysis in adults and second-most common in children
  • Causes problems with eye movements
116
Q

ABDUCENS NERVE PALSY - CAUSE

A
  • Caused by damage to the sixth cranial nerve or obstruction anywhere along its path from the brainstem to the eye
117
Q

ABDUCENS NERVE PALSY - POPULATION AFFECTED

A
  • Anyone can be affected
  • Especially those who have had a brain injury or stroke
118
Q

ABDUCENS NERVE PALSY - RISK FACTORS

A
  • Head injury
  • Stroke
  • Having another underlying health condition
  • Diabetes
  • MS
  • Infection
119
Q

ABDUCENS NERVE PALSY - CLINICAL PRESENTATION

A
  • Because each eye has its own lateral rectus muscle and sixth cranial nerve, sixth nerve palsy can affect one or both eyes.
  • Symptoms and the severity of the condition depend on whether both eyes are affected.
  • Double vision.
  • Poor eye alignment or strabismus.
  • Head movement to maintain vision.
  • Headache
  • Nausea
  • Vomiting
  • Papilledema or swelling of the optic nerve
  • Vision loss
  • Hearing loss
120
Q

FACIAL NERVE PALSY - DEFINITION

A
  • Causes sudden weakness in muscle of one side of face
121
Q

FACIAL NERVE PALSY - CAUSES

A
  • Often related to viral infection
122
Q

FACIAL NERVE PALSY - POPULATION AFFECTED

A
  • Pregnant people, diabetic people
123
Q

FACIAL NERVE PALSY - RISK FACTORS

A
  • Pregnancy- especially third trimester
  • Have upper respiratory infection- such as flu or cold
  • Have diabetes
  • Have high blood pressure
  • Obesity
124
Q

FACIAL NERVE PALSY - CLINICAL PRESENTATION

A
  • Rapid onset of mild weakness to total paralysis of one side of face
  • Facial droop and difficulty making facial expressions
  • Drooling
  • Pain around jaw or behind ear
  • Inc sensitivity to sound on affected side
  • Headache
125
Q

DIZZINESS AND VERTIGO (CN8) - DEFINITION

A
  • Dizziness is a term used to describe a range of sensations, such as feeling faint, woozy, weak or unsteady
  • Vertigo is a sensation of whirling and loss of balance, associated particularly with looking down from a great height, or caused by disease affecting the inner ear or the vestibular nerve; giddiness.
126
Q

DIZZINESS AND VERTIGO (CN8) - CAUSE

A
  • Inner ear problems - house sensors that help detect gravity and back and fourth motion
  • Eyes - help determine where body is in space
  • Sensory nerves - sends messages to brain about body movements and positions
  • Circulation problems that cause dizziness - drop in blood pressure, poor blood circulation
  • Neurological conditions - e.g., Parkinson’s
  • Damage to CN8
127
Q

DIZZINESS AND VERTIGO (CN8) - POPULATION AFFECTED

A
  • Can happen at any age, more common in people over 65
128
Q

DIZZINESS AND VERTIGO (CN8) - RISK FACTORS

A
  • Older adults
  • Past episodes of dizziness
129
Q

DIZZINESS AND VERTIGO (CN8) - CLINICAL PRESENTATION

A
  • False sense of motion or spinning (vertigo)
  • Light-headedness of feeling faint
  • Unsteadiness or loss of balance
  • Feeling of floating, wooziness or heavy headedness
130
Q

MYASTHENIA GRAVIS - DEFINITION

A
  • Characterised by weakness and rapid fatigue of any muscle under voluntary control
131
Q

MYASTHENIA GRAVIS - CAUSE

A
  • Antibodies- Immune system produces antibodies that blocks or destroys muscle receptor sites for neurotransmitter acetylcholine
  • Thymus gland - Believed that thymus gland can trigger or maintain production pf antibodies which block Ach
  • Mother to child - if treated promptly child usually recovers within two months after birth
132
Q

MYASTHENIA GRAVIS - POPULATION AFFECTED

A
  • Women more likely under 40
  • Men over 60
133
Q

MYASTHENIA GRAVIS - RISK FACTORS

A
  • Women between 20-30
  • Men 60-70
134
Q

MYASTHENIA GRAVIS - CLINICAL PRESENTATION

A
  • Muscle weakness worsens as affected muscle is used
  • Usually improves with rest
  • Muscle weakness can come and go
  • Eye muscles - Usually first sign, Drooping of one or both eyelids, Double vision
  • Facial and throat muscles - Impaired speaking, Difficulty swallowing, Affects chewing, Changes facial expressions
  • Neck and limb muscles - General weakness, Can affect walking, Weak neck muscles make it hard to hold head up
135
Q

ACOUSTIC NEUROMA - DEFINITION

A
  • Noncancerous, slow-growing tumour that develops on vestibular nerve leading from inner ear to brain
136
Q

ACOUSTIC NEUROMA - CAUSE

A
  • Linked with defect of gene on chromosome 22
  • Normally this gene produces tumour suppressor protein that helps control growth of Schwan cells covering nerves
  • Most cases, no known cause
137
Q

ACOUSTIC NEUROMA - POPULATION AFFECTED

A
  • Women between 30 and 60
138
Q

ACOUSTIC NEUROMA - RISK FACTORS

A
  • Neurofibromatosis type 2- parent with rare genetic disorder neurofibromatosis type 2
139
Q

ACOUSTIC NEUROMA - CLINICAL PRESENTATION

A
  • Easy to miss and may take years to develop
  • Hearing loss- usually gradually worsening over months to years
  • Tinnitus
  • Unsteadiness/loss of balance
  • Vertigo
  • Facial numbness/loss of muscle movement
140
Q

BENIGN PAROXYSMAL POSITIONAL VERTIGO (BPPV) - DEFINITION

A
  • Most common cause of vertigo
141
Q

BENIGN PAROXYSMAL POSITIONAL VERTIGO (BPPV) - CAUSE

A
  • Idiopathic
  • Associated with minor to severe blow to head
142
Q

BENIGN PAROXYSMAL POSITIONAL VERTIGO (BPPV) - POPULATION AFFECTED

A
  • Women over 50
143
Q

BENIGN PAROXYSMAL POSITIONAL VERTIGO (BPPV) - RISK FACTORS

A
  • 50+
  • Women
  • Head injury
144
Q

BENIGN PAROXYSMAL POSITIONAL VERTIGO (BPPV) - CLINICAL PRESENTATION

A
  • Dizziness
  • Vertigo
  • Loss of balance/unsteadiness
  • Nausea/vomiting
  • Come and go, commonly last less than one minute
145
Q

LABARYNTHITIS - DEFINITION

A
  • Inflammation of labyrinth - part of inner ear
  • Inner ear infection - responsible for hearing and balance
146
Q

LABARYNTHITIS - CAUSE

A
  • Mostly caused by virus, sometimes bacteria
147
Q

LABARYNTHITIS - POPULATION AFFECTED

A
  • Adults 30 to 60
148
Q

LABARYNTHITIS - RISK FACTORS

A
  • Drinking large amounts of alcohol
  • Fatigue
  • History of allergies
  • Recent viral illness, respiratory infection, or ear infection
  • Smoking
  • Stress
  • Using certain prescription or nonprescription medicines (such as aspirin)
149
Q

LABARYNTHITIS - CLINICAL PRESENTATION

A
  • Loss of balance
  • Dizziness
  • Vertigo
  • Nausea/vomiting
  • Blurry vision
  • Hearing loss
  • Tinnitus
150
Q

MENIERE’S DISEASE - DEFINITION

A
  • Inner ear problem that can cause vertigo and hearing loss
151
Q

MENIERE’S DISEASE - CAUSE

A
  • Unknown
  • May be due to extra fluid in inner ear called endolymph
152
Q

MENIERE’S DISEASE - POPULATION AFFECTED

A
  • Usually starts between 40-60
153
Q

MENIERE’S DISEASE - RISK FACTORS

A
  • Family Hx
  • Pressure changes
  • Stress
  • Changes hormones
  • Problems sleeping
154
Q

MENIERE’S DISEASE - CLINICAL PRESENTATION

A
  • Regular dizzy spells
  • Hearing loss
  • Ringing in ear
  • Feeling of fullness in ear
155
Q

VESTIBULAR MIGRAINE - DEFINITION

A
  • Nervous system problem that causes vertigo in people who have a Hx of migraine symptoms
156
Q

VESTIBULAR MIGRAINE - CAUSE

A
  • Unsure
  • Potential misfires between nerve cells in brain
157
Q

VESTIBULAR MIGRAINE - POPULATION AFFECTED

A
  • More common in women around 40
158
Q

VESTIBULAR MIGRAINE - RISK FACTORS

A
  • Mood- stress/anxiety
  • Poor sleep
  • Dehydration/hunger
  • Dietary triggers- e.g., caffeine
  • Hormonal changes
159
Q

VESTIBULAR MIGRAINE - CLINICAL PRESENTATION

A
  • Headaches and dizziness which comes and goes
  • Nausea and vomiting
  • Balance problems
  • Sensitivity to sound
160
Q

UPPER MOTOR NEURON LESION

A

Upper motor neurons originate in the cerebral cortex and descend through the spinal cord, where they interact with lower motor neurons

161
Q

UPPER MOTOR NEURON LESION - S&S

A
  • Weakness with minimal or absent associated atrophy
  • Hyperactive reflexes
  • Increased muscle tone
  • Spasticity
  • Rigidity
  • Minimal paralysis of voluntary movement
  • Tremor
  • Chorea
    • Random involuntary contractions of the extremities
  • Athetosis
    • Slow, irregular movements in the distal extremities
  • Dystonia
    • Sustained, involuntary twisting movements
  • Positive Babinski’s and Hoffman’s reflexes
162
Q

GLAUCOMA - DEFINITION

A
  • Group of eye conditions that damage the optic nerve
  • The optic nerve sends visual information from your eye to your brain and is vital for good vision
163
Q

GLAUCOMA - CAUSE

A
  • Glaucoma develops when the optic nerve becomes damaged
  • As the nerve gradually deteriorates, blind spots develop in your vision
  • This nerve damage is usually related to increased pressure in the eye
164
Q

GLAUCOMA - POPULATION AFFECTED

A
  • People from black, Asian and Hispanic heritage over 40
  • All other people over 60
165
Q

GLAUCOMA - RISK FACTORS

A
  • High internal eye pressure, also known as intraocular pressure
  • Age over 55
  • Black, Asian or Hispanic heritage
  • Diabetes
  • Migraines
  • High blood pressure
  • Sickle cell anaemia
  • Corneas that are thin at the centre
  • Extreme near-sightedness or farsightedness
  • Eye injury or certain types of eye surgery
  • Taking corticosteroid medications, especially eye drops, for a long time
166
Q

GLAUCOMA - CLINICAL PRESENTATION

A
  • Open angle glaucoma
    • No symptoms in early stages
    • Gradually, patchy blind spots in the peripheral vision
    • In later stages, difficulty seeing things in your central vision
  • Acute angle-closure glaucoma
    • Severe headache
    • Severe eye px
    • Nausea or vomiting
    • Blurred vision
    • Halos or coloured rings around lights
    • Eye redness
  • Normal-tension glaucoma
    • No symptoms in early stages
    • Gradually blurred vision
    • In later stages, loss of side vision
  • Glaucoma in children
    • Dull or cloudy eye (infants)
    • Increased blinking (infants)
    • Tears without crying (infants)
    • Blurred vision
    • Near sightedness that gets worse
    • Headache
  • Pigmentary glaucoma
    • Halos around lights
    • Blurred vision with exercise
    • Gradual loss of peripheral vision
167
Q

PAPILLEDEMA - DEFINITION

A
  • Medical term for swelling of the optic disc
  • Almost always bilateral
168
Q

PAPILLEDEMA - CAUSE

A
  • High intracranial pressure causes papilledema
169
Q

PAPILLEDEMA - POPULATION AFFECTED

A
  • Overweight women
170
Q

PAPILLEDEMA - RISK FACTORS

A
  • Space occupying lesions
  • Risk factors for idiopathic intracranial hypertension include
    • Recent weight gain
    • Underlying associated conditions
      • Polycystic ovarian syndrome
      • Anaemia
      • Thyroid disease
      • Sleep apnoea
171
Q

PAPILLEDEMA - CLINICAL PRESENTATION

A
  • Some people have no symptoms
  • Headaches
    • May be worse in the mornings or when lying down
  • Transient visual obscuration’s
    • Periods of about 5 to 15 seconds when vision gets blurry, goes grey or blacks out
    • Usually happen when you change posture
    • Can be unilateral or bilateral
  • Diplopia
  • Nausea
  • Vomiting
  • Neurological symptoms
    • May include problems with movement or thinking
  • Vision loss worsens as the condition progresses
172
Q

OPTIC NEURITIS - DEFINITION

A
  • Occurs when inflammation damages the optic nerve
173
Q

OPTIC NEURITIS - CAUSE

A
  • Exact cause is unknown
  • Believed to develop when the immune system mistakenly targets the substance covering the optic nerve, resulting in inflammation and damage to the myelin
  • The following autoimmune conditions are associated with optic neuritis
    • Multiple sclerosis
    • Neuromyelitis optica
    • Myelin oligodendrocyte glycoprotein (MOG) antibody disorder
174
Q

OPTIC NEURITIS - POPULATION AFFECTED

A
  • Females aged 20-40
175
Q

OPTIC NEURITIS - RISK FACTORS

A
  • Age - Adults 20 – 40
  • Sex - Women much more likely
  • Race - Occurs more often in white people
  • Genetic mutations
176
Q

OPTIC NEURITIS - CLINICAL PRESENTATION

A
  • Usually only affects one eye
  • Pain - Often worsened by eye movement, often a dull achey pain
  • Vision loss in one eye
    • Most people have at least some temporary reduction in vision, but the extent of loss varies
    • Noticeable vision loss usually develops over hours or days and improves over several weeks to months
    • Vision loss is permanent in some people
  • Visual field loss - Side vision loss can occur in any pattern, such as central vision loss or peripheral vision loss
  • Loss of colour vision - Often affects colour perception, may notice colours appear less vivid than normal
  • Flashing lights
177
Q

OPTIC NERVE ATROPHY - DEFINITION

A
  • Optic atrophy is a condition where the cranial nerve wastes away or deteriorates
  • The cranial nerve carries impulses from the eye to the brain
178
Q

OPTIC NERVE ATROPHY - CAUSE

A
  • Where something interferes with the optic nerves ability to transmit impulses
  • Not a condition within itself but is due to a more serious condition
  • The interference can be caused by numerous factors; including
    • Glaucoma
    • Stroke of the optic nerve
      • Anterior ischemic optic neuropathy
    • A tumour that is pressing on the optic nerve
    • Optic neuritis
    • A hereditary condition in which the person experiences loss of vision first in one eye, and then in the other
    • Improper formation of the optic nerve
179
Q

OPTIC NERVE ATROPHY - POPULATION AFFECTED

A
  • White people aged 10 – 50
180
Q

OPTIC NERVE ATROPHY - RISK FACTORS

A
  • High cholesterol
  • High blood pressure
  • Sudden drop in blood pressure or blood loss
  • Swollen arteries in the head
  • Clogged arteries
  • Heart disease
  • Diabetes
  • Sleep apnoea
  • Smoking
  • Migraines
  • Glaucoma
181
Q

OPTIC NERVE ATROPHY - CLINICAL PRESENTATION

A
  • Symptoms relate to a change in vision
  • Blurred vision
  • Difficulties with peripheral vision
  • Difficulties with colour vision
  • Reduction in sharpness of vision
182
Q

OPTIC NERVE NEUROPATHY - DEFINITION

A
  • Sudden loss of vision due to an interruption of blood flow to the anterior of the optic nerve
  • 2 types
    • Arteritic AION
    • Nonarteritic AION
183
Q

OPTIC NERVE NEUROPATHY - CAUSE

A
  • Arteritic AION
    • Dangerous condition
    • Caused by inflammation of arteries supplying blood to the optic nerve - inflammation is due to giant cell arteritis or temporal arteritis
  • Nonarteritic AION
    • Most common form of AION
    • Caused by one of the following
      • A drop in blood pressure to such a degree that blood supply to the optic nerve is decreased
      • Increased pressure inside the eyeball
      • Narrowed arteries
      • Increased blood viscosity
      • Decreased blood flow to the optic nerve where it leaves the back of the eye
184
Q

OPTIC NERVE NEUROPATHY - POPULATION AFFECTED

A
  • Adults over 50
  • A-AION – women more than men (3x)
185
Q

OPTIC NERVE NEUROPATHY - RISK FACTORS

A
  • High blood pressure
  • Diabetes mellitus
  • High cholesterol
  • Smoking
  • Sleep apnoea
  • Heart disease
  • Blocked arteries
  • Anaemia or sudden blood loss
  • Sudden drop in blood pressure
  • Sickle cell trait
  • Vasculitis
186
Q

OPTIC NERVE NEUROPATHY - CLINICAL PRESENTATION

A
  • Main symptoms of NA-AION is
    • Sudden, painless loss or blurring of vision in one eye
    • Decreased visual activity
    • Dyschromatopsia
    • Relative afferent pupillary defect
    • Swollen optic nerve with splinter haemorrhages
    • Visual field defect
  • Main symptoms of A-AION are the same as Giant Cell Arteritis
  • S&S of GCA
    • Pain in the temples
    • Pain when chewing
    • Scalp pain or tingling
    • Neck pain
    • Muscle aches and pains - Esp in upper legs or arms
    • General fatigue
    • Loss of appetite
    • Unexplained loss of weight
    • Fever
187
Q

MACULAR DEGENERATION - DEFINITION

A
  • Also known as age-related macular degeneration
  • An eye disease that affects central vision
188
Q

MACULAR DEGENERATION - CAUSE

A
  • Inherited eye disease
  • Occurs when the macula at the back of the eye starts to deteriorate for an unknown reason
  • Dry
    • Develops when tiny yellow protein deposits called drusen form under the macula
  • Wet
    • Occurs when abnormal blood vessels develop under the retina and macula and the blood vessels leak blood and fluid
189
Q

MACULAR DEGENERATION - POPULATION AFFECTED

A
  • White people over 50
190
Q

MACULAR DEGENERATION - RISK FACTORS

A
  • Older age - Over 50
  • Family hx
  • Being overweight
  • Smoking
  • Hypertension
  • Diet high in saturated fats
  • Being of European descent
191
Q

MACULAR DEGENERATION - CLINICAL PRESENTATION

A
  • Many people don’t have symptoms until the disease progresses
  • Blurred vision
  • Blank or dark spots in field of vision
  • The appearance of waves or curves in straight lines
192
Q

DIABETES AND THE OPTIC NERVE

A
  • Diabetes can damage the eyes over time and cause vision loss, even blindness
  • Eye diseases that can affect people with diabetes include
    • Diabetic retinopathy
    • Macular oedema
    • Cataracts
    • Glaucoma
  • Early diagnosis and treatment can go a long way toward protecting eyesight
  • Managing diabetes and getting regular eye tests can prevent these conditions
193
Q

MULTIPLE SCLEROSIS AND THE OPTIC NERVE

A
  • Visual problems is the first sign of MS in many people
  • Eye diseases that can affect people with MS include
    • Optic neuritis
    • Nystagmus
    • Diplopia
  • Prognosis is good for recovery from many vision problems associated with MS
194
Q

HYPERTENSION AND THE OPTIC NERVE

A
  • High blood pressure can damage the tiny, delicate blood vessels that supply blood to the eyes
  • This can cause
    • Retinopathy
      • Damage to the blood vessels in the retina
    • Choroidopathy
      • Fluid build-up under the retina
    • Optic neuropathy
      • Nerve damage
    • Treatment and lifestyle changes can help control high blood pressure and reduce the risk of developing these eye diseases
195
Q

B12 AND THE OPTIC NERVE

A
  • Vitamin B12 plays an important role in the production of red blood cells
  • It helps create and regulate DNA and aids in the function of brain cells
  • Can cause
    • Disturbed or blurred vision
    • Optic neuropathy
  • Happens when the deficiency causes damage to the optic nerve that leads to your eyes

SYSTEMIC CONDITIONS (13 decks)

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