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What is the GCS?
How is the GCS score measured?
Describe the ranges and classifications of brain injury with GCS
- The Glasgow Coma Scale or GCS is a neurological scale that aims to give a reliable, objective way of recording the conscious state of a person for initial as well as subsequent assessment. There are 3 parameters out of 4, 5 and 6 respectively (lower the score the more "unconscious")
- - Eyes: doesn't open eyes to opens eyes spontaneously
- - Verbal: from no sounds made to being orientated and normally conversing
- - Motor: Makes no movements to obeying commands
- *Should have a skim over the other numbers
- Mild Traumatic Brain Injury (Glasgow Coma Scale score 13-15)
- Moderate Traumatic Brain Injury (Glasgow Coma Scale core 9-12)
- Severe Brain Injury (GCS lower than 9)
(a) GCS is important in assessment of traumatic head injury but less useful in assessing other forms of neurological impairment. Why?
(b) List the defining features of deep unconsciousness/coma. How do these differ in someone who is simply asleep?
- The score was devised to evaluate levels of consciousness from fully conscious and interacting with the environment through to non-response coma or death.
- - other neurological functions require (or at least it is assumed) that the patient is fully conscious; i.e. memory, personality, intelligence tests etc.
- In coma or deep unconsciousness we are unable to react to the environment. In this state;
- - people are not rousable
- - there is no sleep-type EEG activity
- - there is low brain metabolic activity
- - decorticiate/decerebrate posture: an abnormal body posture that involves the arms and legs being held straight out, the toes being pointed downward, and the head and neck being arched backwards. The muscles are tightened and held rigidly.
3(a) From your learning about the consequences of brain injury in the Behavioural Sciences Module, list four patient-related factors which increase the risk of problems after brain injury. (5 minutes)
3(c) Given the seriousness of Molly’s brain injury name five common cognitive symptoms that you would expect to see in Molly in the long term. Describe each symptom in a lay person’s words (i.e. as you would explain each of them to Molly’s parents). (10 min)
- a) increasing the risk of poor outcomes after TBI is young age (however more likely to make recovery), lack of social support, previous psychological comorbidity such as depression or substance abuse, previous head injury, below 2 years or over 60 years
- Fatigue - will get tired easily. Her most productive times will be in the morning
- Memory loss - she may be quite forgetful at times
- Irritability - she may lose her temper from time to time, especially when she is fatigued
- Impaired concentration - she may find it harder to listen for long periods of time
- Deficits in executive functioning - much like teenagers she may have trouble making what we would call "mature decisions"
- Communication problems - she may have trouble holding a conversation
3(a) From your learning about the long term consequences of brain injury in the Behavioural Medicine module, briefly describe four important features related to children with head injuries which differentiate them from adults with head injuries
3(b) What is the most important thing for Lilly's family doctor to keep in mind in order to provide optimal care to a young child with brain injuries such as Lilly?
- 3 (a) Larger heads in proportion to body size so more prone to injury
- - Developing brain - critical period can result in worse damage
- - Brain is more plastic so may be able to recover better ?
- - Thinner skull
- - Latency; Problems may become evident after a long period of time when social differences become more noticeable
- 3 (b) Make sure she is getting lots of sleep and not over working her brain so it has a chance to heal.
- - Keep her Mother informed and make sure she informs the relevant people at school for two reasons; one she may need extra support, two head injuries are a silent epidemic and it is important that class mates and teachers alike are more understanding
What are the possible long-term effects (personal, psychological, family, spiritual) of such a brain injury? (15 minutes)
- Most brain injuries are mild and do not cause permanent or long-lasting disability but all levels of severity have the potential to cause significant, long-lasting disability. Even a mild TBI can affect memory, dizziness and fatigue for several years after injury.
- *Think about what happened to Grandma*
- Physical: problems with movement, speech, senses, dizziness (especially with cerebellar involvement), headaches
- Cognitive: memory loss is the most common long-term affect, fatigue (especially mental fatigue) is also a common feature of TBI, impaired attention, concentrating problems, distractibility, deficits in executive functioning
- Social: changes in personality, especially inappropriate social or sexual behaviour, impulsiveness, disinhibition, poor social judgement
- Emotion and Behaviour: increased irritability, anger (especially explosive temper), depression, anxiety, mania, apathy, OCD, failure to initiate, lack or persevering, low motivation, poor insight, increased risk of self-harm or suicide
- Relationships: changes in relationships with intimate partners, family members and friends, family members may have to take on the role of care-giver which forces them to sacrifice their own relationships, employment, leisure activity, etc.
- - changes in the sexual relationship if a partner has to become a care-giver
- Financial: loss of income, inability to return to work, difficulty securing employment, difficulty remaining employed or coping with the demands of work, reduction in status and previous abilities
- Quality of Life: increased isolation, grief and loss of previous abilities, skills, relationships, activities
- Spiritual: loss of meaning in life, blame, crisis of faith, lost connection with self and spirit
Whilst on the ward Mr Walker has a seizure. This begins with jerking of his left arm and proceeds to loss of consciousness and generalised convulsions.
1(a) How do you classify epileptic seizures? (6 minutes)
1(b) What type of seizure has Mr Walker had? (2 minutes)
1(c) In general why does classification of seizures matter? (2 minutes)
- (a) There are three classifications for epileptic seizures:
- 1. Partial (focal, local) seizures: These begin in a specific area of the brain and may be contained or spread to the entire brain. There are 2 subtypes
- - simple partial seizures: the person remains conscious
- - complex partial seizures: involve impaired consciousness
- Simple partial seizures may evolve into complex partial seizure. Both may evolve into a secondarily generalized seizures (usually tonic-clonic)
- 2. Generalized seizures
- These involve both sides of the brain from the start of the attack
- - absence seizures (petit mal): can be typical or atypical and involving a brief loss of consciousness
- - myoclonic: sporadic (isolated), jerky movements
- - clonic: repetitive, jerking movements
- - tonic: muscle stiffness, rigidity
- - tonic-clonic (grand-mal): unconsciousness, convulsions, muscle rigidity
- - atonic: loss of muscle tone
- 3. Unclassified seizures
1(b) He has experienced a partial seizure initially
(jerking of his left arm initially) that has evolved to a tonic-clonic generalized seizure
(proceeds to loss of consciousness and generalised convulsions).
- 1(c) Classification of seizures influences choice of treatment. For example;
- - Cabamazepine, valproate and phenytoin can control tonic-clonic seizures 70 - 80% of the time but are only effective for partial seizures 30 - 40 % of the time. Other drugs are more effective here
Lilly was having funny turns;
- episodes of staring blankly followed by isolated jerks of the upper lip
EEG confirmed increased activity
2(a) What is the likely diagnosis for Lilly? (2 minutes)
2(b) What drug treatment options would you consider? (3 minutes)
2(c) What would be the likely adverse side effects of these treatments? (5 minutes)
2(d) How would you manage these side effects? (5 minutes)
- Epilepsy: complex (loss of consciousness), partial (1 part of the brain - lip twitch) seizure involving staring episodes and progressing to myotonic jerks
- Valproate: good for infants and against absence seizures. Carbamazepine could be good too as it is suitable for partial complex seizures
- Adverse effects: Liver enzymes increasing, GI upset, weight gain, decrease platelets
- Managing side effects: Ensure they're on the minimum correct dose, with regular tests levels to ensure they are within the therapeutic range
- - Keep communication lines open with the patient so that they can feel free to change medication if the side effects are too much - this will help to remove problems with adherence
- - Anti-emetics for nausea
- - Special diet for GI problems and weight gain
- - Regular checks of liver function and platelet counts
- - May need to try a few different drugs to see what the patient prefers
A nurse noticed that Molly was having a seizure.
2(a) (5 minutes)
(i) What drug treatment would be appropriate to manage Molly’s seizure?
(ii) What drug treatment would be appropriate should she require ongoing prophylaxis for seizures?
2(b) Outline the mechanisms of action and the adverse side effects of the drugs you identified in
(i) and (ii) above. (5 minutes)
2(a) Treatment should consider cause of seizure
(e.g. manitol if it is ICP causing pressure)
- Phenytoin is good for prevention of seizure post neurosurgery
- - It is a barbiturate derivative and is still widely used, except for absence seizures.
- Pharmacokinetics: narrow range of plasma concentrations to cause adverse side effects
- - hence therapeutic drug monitoring (TDM) is essential
- Mechanism/Target: blocks voltage-gated sodium channels by selectively binding to the channel in the inactive state and slowing its rate of recovery.
- - prolongs effective refractory period and suppresses ventricular pacemaker automatically, and shortens action potential in the heart
- Adverse effects: Decreased bone mineral density
- - suicidal ideations
- - Can be associated with fetal abnormalities
- Carbamazepine (Tegritol TM ) also Na+ channel blocker (similar to phenytoin), especially good against complex partial seizures
- - Side effects - nausea, headache, rash, dizziness, double-vision
- - Potent enzyme inducer, difficult to titrate. Interacts with numerous other common drugs.
- - May lead to SIADH as it increases release of ADH. Causes reduction in blood cells and platelets. Induces CYP450 so multiple drug interactions including birth control pills. Teratogen.
shows zero-order (saturation) kinetics; clearance is independent of plasma conc, duration of drug action dependent on dose, relationship between dose and steady-state conc steep and unpredictable. plus everyone responds differently to this drug!
Compare and contrast the older anti epileptic drugs (AED’s) phenytoin, carbamazepine, phenobarbitone and diazepam in terms of their mechanisms of action, efficacy and advantages/disadvantages in the treatment of epilepsy.
- Phenobarbitone (a barbiturate) and diazepam (a benzodiazepine) are two of the “older” AED’s.
- Both are allosteric modulators of the GABA-A receptor and enhance Cl-conductance through the channel when the receptor is activated by GABA. Both are good for many seizure types.
- - Unfortunately both drugs are highly sedative and addictive.
- - Diazepam is especially useful in that it has a very rapid action and can be used to quickly control status epilepticus.
*Extra credits: teratogenecity, enzyme induction, clearance, T1/2 and dosing,
Mr EG has a seizure described as; "twitching movements began in his left hand, then spread proximally to involve the left wrist, elbow and then shoulder"
Describe in detail, at both the gross anatomical and the cellular level, the neuroanatomical structures and pathways by which abnormal activity in the cerebral cortex would result in contractions of the specific muscles initially involved in Mr EG’s seizure. Your answer should include details of both cortical organization, and of the pathway from cortex to muscle. Illustrate your answer with at least one diagram.
- Abnormal firing in sequence of populations of neurons in the precentral gyrus of the motor cortex on the right side of the brain.
- The abnormal firing has spread along the motor homunculus in the precentral gyrus. It has started in the middle of the lateral part of the precentral gyrus where the neurons that control finger movements are located
- - It has then spread superiorly to end near the superior margin of the lateral part of the precentral gryus where the neurons that control shoulder movement are located.
- The abnormally firing neurons would include the Layer V Betz [pyramidal] cells in the right precentral gyrus. These neurons form the corticospinal tract. They send their axons through the corona radiata of the cerebrum, and then the posterior limb of the internal capsule, to enter the middle part of the cerebral peduncle in the anterior part of the midbrain. The axons then course through the anterior part of the pons, and then form the pyramidal tract in the most anterior region of the medulla.
- When the medulla joins the spinal cord, the axons cross-over (decussate) to the left side of the spinal cord and form the lateral corticospinal tract. These axons then descend in the spinal cord to the level of the anterior horn neurons that form the brachial plexus [C5 to T1] and synapse with these anterior horn neurons [via interneurons].
- These neurons send their axons out of the spinal cord via peripheral nerves (LMN) to innervate the muscles of the upper limb.
Describe the neural control mechanisms (somatic, autonomic and brainstem) that combine to allow the bladder to store urine and maintain urinary continence.
How do these mechanisms adjust during micturition?
What part of this system is likely to have been damaged in Mrs Jones’ case?
- Storage / Continence: As bladder fills and stretches;
- - stretch receptors activate the SNS which relaxes the detrusor muscle and adjusts tone so that there is a minimal increase in intra-vesical (bladder) pressure as it fills.
- - reflexes also inhibit pelvic PSNS inputs to detrusor which prevents it from contracting.
- - descending inputs from the lateral pontine micturiton center (LPMC) (aka centre for continence) in the dorsomedial pons enhance these processes
- The external urinary sphincter is kept closed by somatic inputs via motor fibres in the pudendal nerve. These originate in Onuf's nucleus (sacral cord) which is tonically active.
- Sensory fibres from stretch receptors in the bladder wall and descending inputs from LPMC increase Onuf's output to tighten the sphincter as the bladder fills.
- Micturition (Urination): is initiated voluntarily by activity of medial pontine micturition centre MPMC (centre for micturition) which inhibits the LPMC which leads to;
- - decreased activation of Onuf's motorneurons in pudendal nerve -> sphincter opens
- - PSNS mediated reflex contraction of detrusor muscle occurs.
- i.e when want to urinate MPMC “releases” the micturiton reflexes -urine flows – which;
- - when sensed in the urethra stimulates further contraction of detrusor and relaxation of external sphincter.
- - is further increased by relaxation of pelvic floor muscles (perineal, levator ani) which decreases urethral resistance
- - is further increased by voluntary contraction of diaphragm and abdominal muscles which increases intra-abdominal pressure which increases intravesical pressure.
- SNS is not required for micturition – in fact SNS efferent activity in hypogastric nerve is inhibited during bladder emptying.
- Incontinence during seizure activity is multi-factorial:
- - Disruption of ANS will alter SNS & PSNS outputs
- - Activation / relaxation of somatic pathways will affect external urinary sphincter
- - Disruption of brainstem activity i.e MPMC and LPMC with resultant loss of descending control of bladder function.
3(a) Name the three main theoretical components of the memory system. Describe the capacity and duration of storage of each component, and name the process normally used by each component to store information about events for future reference. (7 minutes)
3(b) Give an example of how any ONE of the processes from question 3(a) above might be disrupted by an epileptic seizure. (3 minutes)
- Sensory register (huge capacity, very short duration) attention
- Short term memory (capacity 7 +/-2, duration seconds/minutes) rehearsal/encoding
- Long term memory (unlimited capacity & duration)
- Seizure could affect info arriving from sense organs, so event not perceived; could prevent person paying attention, so event not registered by short term memory, or could prevent rehearsal, so memory not encoded into LTM
Identify the location of the lesion as closely as possible.
(ii) Suggest what neurological functions are most likely to be disturbed by these lesions and explain why, in relation to the structures which may be damaged (do not restrict your answer to the presenting clinical features listed above).
- Lesion 1: white matter of anterior occipital lobe
- - Loss of all or part of left visual field due to damage to the fibres of the optic radiation on the right side, in the occipital region ‘4/5’.
- Lesion 2: White matter just lateral to body of lateral ventricle, on boundary of frontal & parietal lobes (more parietal)
- - Motor & sensory functions of the right side, due to damage to fibres of corona radiata passing to pre-and post-central gyrus; particularly functions of the limbs
- - face probably not affected as these fibres pass more laterally [might also affect long association fibres (superior longitudinal fasciculus) with resulting speech problems, as on left side
What does the temporal appearance of the MRI suggest about the course of the disease?
Give a diagnosis based on the MRI, VEP and clinical findings
- Course: Fluctuating course characterized by acute attacks interspersed with periods of remission.
- - white so they must have a high water content. They most likely represent some kind of inflammatory process which is causing oedema.
- - An inflammatory process which causes focal destruction and subsequent healing of the brain tissue.
- - Because the damage is in the white matter, the damage is likely to have occurred in the axons of the nerves.
- Diagnosis: MS
- What are the Differences Between Multiple Sclerosis and Guillain-Barré Syndrome?
- - Multiple sclerosis and Guillain-Barré are two demyelinating conditions that affect the nervous system. Patients with either of these conditions have a loss of myelin, which covers the axons of the neurons. Both are autoimmune disorders, meaning the immune system attacks the body, resulting in inflammation.
- - they affect different types of myelin. Multiple sclerosis is a demyelinating disease of the central nervous system, which includes the brain and spinal cord. Guillain-Barré is a demyelinating disease of the peripheral nervous system, which are the nerves outside of the brain and spinal cord. The cells are different; CNS myelin is from oligodendroglia and PNS myelin is from Schwann cells.
Give the function of the following;
- *Sclera: tough, white outer covering of the eyeball; extraocular muscles attach here to move the eye
- * Choroid: Thin tissue, layer containing blood vessels, sandwiched between the sclera and retina; also, because of the high melanocytes content, the choroid acts as a light-absorbing layer.
- Retina: layer of tissue on the back portion of the eye that contains cells responsive to light (photoreceptors)
- Fovea: surrounded by the macula where there is a large density of photo-receptors but little vasculature- Macular degeration occurs with death or impairment of functioning of the photoreceptor cells in this region, leading to central vision and colour acuity loss.
- Optic disk and Optic nerve: and retinal vessels. No photoreceptors which causes the blind spot
- - The subarachnoid space surrounding the optic nerve is continuous with that of the brain; as a result, increases in intracranial pressure—a sign of serious neurological problems such as a space-occupying lesion—can be detected as papilledema, a swelling of the optic disk.
What are the main differences between rods and cone receptors?
- Rods are the more abundant receptor especially in parts of the retina associated to peripheral vision, and have a relatively low spatial resolution but are far more sensitive to light compared to cones- therefore are predominantly used in the dark (scotopic conditions).
- - retina has mostly rods (95%), the center of the fovea, which is the part of the retina that mediates acute vision, has exclusively cones.
- - There is only one variant of the rod receptors
- Cones have high spatial vision during the day and they are important in the sensation of colour. They have dense resolution but are not as sensitive to light (25–100 times less)- making it more suited for acuity rather than sensitivity.
- - Cones are predominantly situated at the fovea/macula of the retina.
- - Cones exist in three varieties which include photopigments specific to different ranges in wavelengths; Short wavelength cones (S) for blue, Medium (M) wavelength cones for green and Long (L) wavelengths for red
- Both rods and cones hyperpolarise to a light increment
How does signal transduction occur in the visual sensory system? Describe the chain of events in the amplification cascade
- Phototransduction in rodphotoreceptors 1: Rhodopsin
- Opsin is a molecule which sits the membrane of the phororeceptors; not the cell membranes but the "disk" membranes within the cells which line up parallel with eachother and perpendicular to the light incidence.
- 11-cis retinal: when a photon of light hits this molecule, it undergoes an energetic conversion to an all-trans form which causes a slight conformational change. This initiates a cascade of biochemical events which help with signal transduction
- (1) Photon is captured by rhodopsin
- (2) The rhodopsin adopts a photoexcited state
- (3) intracellular messenger, Transducin
- (4) activated phosphodiesterase
- (5) hydrolylis of cyclic guanosene monophosphate; cGMP → 5'GMP
- (6) ↓cGMP closes Na+ channels → Membrane hyperpolarised by ~ 1mV causing a x200 increase in amplitude from the initial stimulus
Summarise the cellular pathway in the retina from the light receptor cells to the output axons of the optic nerve.
- Can get a bit complicated at the level of the retina; photoreceptor to bipolar cell to ganglion cell at its simplist
- Ganglion cells make up the optic nerve and travel out of the retina.
- - they run a straight course to the optic chiasm at the base of the diencephalon. In humans, about 60% of these fibers cross in the chiasm, while the other 40% continue toward the thalamus and midbrain targets on the same side.
- Once past the chiasm, the ganglion cell axons on each side form the optic tract, which hence contain fibers from both eyes.
- - destined for several structures in the diencephalon and midbrain (mainly the dorsal lateral geniculate nucleus of the thalamus)
- Neurons in the lateral geniculate nucleus, like their counterparts in the thalamic relays of other sensory systems, send their axons to the cerebral cortex via the internal capsule.
- These axons pass through the retrolentiform limb of the internal capsule called the optic radiation and terminate in the primary visual cortex
- - which lies largely along and within the calcarine fissure in the occipital lobe.
Identify what impairments would occur with lesions in the following places;
- (A) Loss of vision in right eye.
- (B) Bitemporal (heteronomous or non-overlapping) hemianopsia (i.e. temporal fields of both eyes)
- (C) Left homonymous hemianopsia; e.g. with an expanding aneurysm of the middle cerebral artery, on the right side of the brain.
- (D) Left superior quadrantanopsia.
- (E) Left homonymous hemianopsia with macular sparing.
- - i.e. loss of vision throughout wide areas of the visual field, with the exception of foveal vision. Macular sparing is commonly found with damage to the cortex
Draw the neural pathway for the light reflex and indicate where the damage is likely to have occurred if Mrs Clarkson exhibits a consensual but not a direct light reflex. Briefly explain your reasoning.
- The pupillary light reflex is the reduction in the diameter of the pupil that occurs when sufficient light falls on the retina.
- The initial component of the pupillary light reflex pathway is a bilateral projection from the retina to the pretectum (a midbrain structure).
- - Pretectal neurons → Edinger-Westphal nucleus (a small group of nerve cells that lies close to the nucleus of the oculomotor nerve CN III).
- The Edinger-Westphal nucleus contains the preganglionic parasympathetic neurons that send their axons via the oculomotor nerve to terminate on neurons in the ciliary ganglion.
- Neurons in the ciliary ganglion innervate the constrictor muscle in the iris, which decreases the diameter of the pupil when activated.
- An important diagnostic tool that allows the physician to test the integrity of the visual sensory apparatus, the motor outflow to the pupillary muscles, and the central pathways that mediate the reflex.
- Under normal conditions, the pupils of both eyes respond identically, that is, light in one eye produces constriction of both the stimulated eye (the direct response) and the unstimulated eye (the consensual response). Comparing the response in the two eyes is often helpful in localizing a lesion. For example;
- - a direct response in the left eye without a consensual response in the right eye suggests a problem with the visceral motor outflow to the right eye, possibly as a result of damage to the oculomotor nerve or Edinger-Westphal nucleus in the brainstem.
- - Failure to elicit a direct response in the left eye, whilst both eyes respond normally to stimulation of the right eye (i.e. consensual response) suggests damage to the sensory input from the left eye, possibly to the left retina or optic nerve.
(i) What physiological events contribute to the normal latency from visual stimulus to VEP response measured at the scalp? (4 minutes)
(ii) What pathological process is most likely to account for the increased latency of the VEP in the patient? (1 minute)
- (i) Photoreceptor activation in cones or rods; synaptic transmission in retina; action potential conduction in optic nerve; synaptic transmission in LGN; action potential conduction in optic tract; synaptic transmission in cerebral cortex.
- (ii) Demyelination in optic pathway
What type of motor disorder (upper or lower motor neuron) is suggested by this clinical examination? Justify your answer by comparing the signs typical of upper versus lower motor neuron disorders.
"Ms KJ, had noticed a weakness in her right foot so she was inclined to stumble, but this also gradually recovered. There had also been a period over which she had needed to pass urine more frequently, with occasional incontinence. She had also had further problems with her vision. On physical examination, there was weakness of the right leg, increased tendon reflexes and a positive Babinski sign."
- Both UMN and LMN disease present with: Weakness, and atrophy
- Upper motor neuron lesion: UMN lesions are typically associated with weakness, increased tendon reflexes, and positive Babinski sign.
- - Other symptoms not mentioned include; increased muscle tone with spastic catch (spasticity), and clonus (i.e. muscular spasm involving repeated, often rhythmic, contractions). There is often mild muscle wasting due to disuse atrophy.
- LMN lesions: are characterized by
- - weakness with reduced tone, reduced reflexes, absent Babinski sign, and eventually severe muscle wasting.
- - Fasciculations are also sometimes present due to denervation (twitches of fibres when still, no need to trigger).
If on MRI, there is no direct infarct in the motor homunculus of the lower limbs (but there is in the upper), why might it be that we have paralysis in both?
- The right upper limb is paralysed due to involvement of the left primary motor area for the arm (mid-lateral region of precentral gyrus) in the region of infarct.
- - This region is normally supplied by the MCA.
- Even though the primary motor area for the right lower limb (in left precentral gyrus on medial aspect of hemisphere) seems not to be involved (it is supplied by the anterior cerebral artery), but the motor fibres descending from this region in corona radiata and internal capsule are within the area of infarct.
Explain the likely origins of the signs and symptoms visible in the tongue and facial muscles.
Right limb paralysis + tongue, when protruded, turned to the right but there was no atrophy.
There was paralysis of the lower facial muscles on the right side but upper facial muscles were fine. Sensation was also reduced on the right side of the body.
- The facial area of the left primary motor cortex (most lateral part of left precentral gyrus, adjacent to lateral sulcus) is involved in the area of the lesion, resulting in an upper motor neuron lesion of the muscles supplied by the brainstem.
- Only the lower facial muscles are paralysed, because the motor neurons supplying the upper face receive input from both hemispheres (so are OK),
- - those supplying the lower face receive only contralateral input.
- The tongue curves to the right because the motor neurons supplying the muscles of the tongue receive a predominantly contralateral input from cortex
- - so with left sided damage, the right sided muscles are weak, and the normal protrusor muscles of the tongue push it to the right.
Outline the physiological basis for the spasticity observed in the limbs of a patient with UMN lesions.
- Muscle tone is largely due to activity in the stretch reflex, involving monosynaptic excitatory inputs to alpha motor neurons from sensory (lα) afferents arising from the muscle spindle.
- The muscle spindle is a length sensor of muscle, which is activated when muscles are lengthened. In upper motor neuron lesions, descending inputs to alpha motor neurons are lost and they subsequently become hypersensitive to the inputs from the muscle spindle.
- - Lengthening of the muscle under decreased cortical inhibition leads to 3 signs; heightened responses in the muscle observed as increased tone, spastic catch on sudden muscle stretch, and heightened tendon tap reflexes.
What somatic sensory modalities are tested in a complete neurological examination?
Briefly describe how each is assessed.
- Light touch: cotton wool (cover main dermatomal areas);
- Pain: pin (sterile needle; do not penetrate skin);
- Position/proprioception: joint rotation (care to avoid pressure);
- Vibration: (tuning fork, bony protuberances)
Stroke patient: List the course of therapy that you consider will offer both immediate and long term appropriate pharmacological management of this patient's condition. Briefly give reasons for your choices.
- Acute oxygen therapy if required: we want to prevent further ischemic/hypoxic damage, so if the patient needs help raising their blood O2 saturation this would be indicated
- IF ISCHAEMIC AND CERTAINLY NOT HAEMORRHAGIC: give thrombolytic drugs such as TPA within 3-6 hours of the infarct
- -if haemorrhagic stroke, then bleeding will be prolonged
- Prophylactic drugs: such as asprin (antiplatelet) and heparin and warfarin (anticoagulant) later when the patient is stable;
- Additional treatments to help prevent recurrence involve reducing risk factors by treating hypertension (beta blockers to lower blood pressure), and giving statins to reduce fatty acid deposition inpatients with high cholesterol or altered lipid profiles.
Describe what characteristics you would expect to observe in Mrs G.F.'s speech and/or language if Broca's area alone had been affected.
What about Wernicke's area?
- Broca's area: is a motor association area involved in creating speech. Broca's area which causes the movement of lips, tongue, and other vocal apparatus to create the speech we hear.
- - Must be on the dominant hemisphere (90% of people = left side). If not, her voice may become monotonic.
- A lesion causes Non-fluent aphasia. This involves;
- - Impaired speech production
- - Difficulty expressing speech
- - Laboured, slow, deliberate speech
- - Grammatically simple, but comprehensible
- Comprehension of speech is OK
- Wernicke's aphasia: Damage to this area results in a fluent aphasia, i.e. The inability to comprehend the meaning of speech. They can construct grammatically correct sentences and speak fluently, but cannot convey the meaning of anything that is said to them.
Compare and contrast the pathological features in the brain that would be seen within a week of the stroke, and at a year following the stroke. Include both the macroscopic and microscopic changes in your answer.
- An infarct changes with time.
- 0-6 hours = macroscopically undetectable *especially if haemorrhagic*
- In the first two days, the tissue becomes pale, soft, and oedematous.
- From 2 to 10 days, the brain becomes gelatinous and friable (easily crumbled),
- - the previously ill-defined boundary between normal and abnormal tissue becomes more distinct as the oedema resolves in the adjacent tissue that has survived.
- On microscopic examination: something happens for each cell type;
- - the cytoplasm of the ischaemic neurons firstly becomes red, and spaces appear in which there is oedematous fluid.
- - As the processes of liquefaction and phagocytosis continue, astrocytes at the edges of the lesion progressively enlarge, divide, and develop gliosis from about the first week.
- By a year, the tissue will have liquefied leaving a fluid-filled cavity.
- - The wall of the cavity is formed by gliosis with new capillaries and a few perivascular connective tissue fibres.
- The most common causes of cerebral infarction in this age group (i.e. elderly) are in situ thrombosis (due to atherosclerosis) or embolization from a distant source. Emboli tend to lodge where blood vessels branch or in areas of pre-existing luminal stenosis.
- If the infarct had become haemorrhagic following dissolution of a thrombus and reperfused by the fresh blood supply, extensive blood extravasation (i.e. lacunar haemorrhage) and resorption of the blood in macrophages would be seen.
First describe what we're seeing.
Describe (or draw and label) the appearances seen in the photograph.
- The photo shows a coronal section of the brain at the level of the caudate nucleus, putamen and globus pallidas. There is also a section of the pons.
- The photograph shows an extensive area of infarction in the territory of the middle cerebral artery.
- Obstruction of the blood vessel: seems to be very proximal, considering that the midline structures are involved.
- Age: The cortex of the affected area shows many petechial haemorrhages, and the white matter still has a similar appearance as that of the unaffected side;
- - these features indicate that this is an early infarction, days old.
- The section of the pons shows a central area of haemorrhage (Duret's haemorrhage).
Postulate a mechanism of death
What clinical signs are there of this form of injury?
- The mechanism of death was, most probably, brain oedema, with transtentorial herniation.
- Evidences of this, in the photograph, are the increased size of the affected hemisphere and the presence of Duret's haemorrhage of the pons, which is caused by compression of the brainstem and traction of the arteries of the posterior circulation, with rupture of the penetrating branches of the basilar artery.
- Clinically, evidences of transtentorial herniation include loss of consciousness due to the involvement of the ascending reticular activating system (ARAS),
- - respiratory arrest due to involvement of respiratory nuclei of the brainstem and
- - Blown pupil: the dilatation of the left pupil, due to compression of the third nerve on the side of herniation.
2013: This is a 5 YOA
Why choose CT over MRI???
What is this injury? Why so?
Explain the anatomical basis for the injury seen int he CT. Use a labeled diagram if you need.
- CTs are cheaper, quicker and less frightening for the patient
- - and has the contrast ability to pick out a bleed vs. bone + brain parenchyma
- - In CTs fresh blood reflects x-rays well so extra radiodense. This cant be matched by MRI
- - CT images bone and calcifications very well (latter useful for some tumours e.g. benign meningiomas)
- - MRIs are better for soft tissue imaging, but in the case of checking for haematomas adds no additional diagnostic value compared to CT
- - metalic debris from crash and MRI not good
- This appears to be a subdural haematoma; because of the sickle shape of the accumulated blood, but also because it appears to cross the periostial boundaries of the parietal and frontal bone. Also as it is not as radiodense, and without a bone fracture, less likely to be epidural
- - other non-specific signs of SOL = the mindline shift towards the patient's left, and a compression of the right ventricle
- The brain has some wiggle-room within the cranial cavity so as to allow for some shock absorption and protection. However the brain is tethered to the dura through "bridging veins" which help drain the deox blood from the brain parenchyma.
- - if the brain moves too much within the cavity, these veins can be shorn or torn which causes bleeding.
- But because this "potential space" (between inner meningeal layer of dura and arachnoid mater) is not teathered to the bone as periosteum, rather is at a level deeper in the meninges
- - furthermore, given the blood is deox plus low pressure , it appears less radiodense and less bulging out.
With respect to epidural haematomas, what are the likely anatomical consequences of raised intracranial pressure?
What are the consequences of tentorial herniation?
- (a) Increased pressure → decreased cranial perfusion and possible ischaemia
- - cerebral oedema and displaced midline, and compressed ventricles
- - herniation of uncus, falcine or coning/ cerebellar tonsil
- - can press on the reticular formation → unconsciousness
- - pyramidal tracts and contralateral paralysis (rarely ipsilateral)
- - press on brainstem and potential cessation of respiration
- - BLOWN PUPIL: pressing on occulomotor nerve, unresponsive to light test
Mr Thomas Swan, is 71-years old. On examination;
- his right eye was deviated laterally and the pupil fixed and dilated.
- right ptosis which he said he has had for about 3 years.
- left lower facial paralysis and a mild left hemiparesis affecting mainly the left arm.
(a) Taking into account the clinical presentation, what is the most likely cause of Mr Swan’s pathology and why? (4 minutes)
- (a) The lesion appears to be a medial brainstem one at the level above the brainstem where we expect the occulomotor nucleus to be. This is because;
- - the occulomotor nucleus (and the associated cranial nerve III) innervate eye muscles in the orbit. With it's dysfunction, and the relative strength of Lateral Rectus and the superior occular muscles the eye is left in a lateral deviation
- - furthermore CNIII innervates the eyelid and certain pupillary reflexes (hence dilation), which are also defective in the patient (hence ptosis)
- - The involvement of the contralateral hemipariesis of the left arm and face (which are two medial brainstem tracts with UMNs) which can be explained by a lesion in the corticospinal and corticobulbar tracts respectively. More specifically, the gracile fasiculus is involved (the arms)
What are the major clinical features that distinguish medial medullary syndrome from lateral medullary syndrome? (8 mins)
- Medial medullary syndrome:
- - Ipsilateral LMN paralysis of tongue (involvement of XII hypoglossus)
- - contralateral hemiparesis of body (gracile affected before cunneate),
- - contralateral loss of fine touch, vibration and proprioception (from medial lemniscus) of body,
- - issues with conjugate gaze due to involvement of medial longitudinal fasiculus
- Lateral medullary syndrome: affected pathways include
- 1.) The Spinocerebellar pathways: ipsilateral ataxia of the arm and leg.
- 2.) The Spinothalamic pathway: contra lateral alteration of pain and temperature affecting the arm, leg and rarely the trunk.
- 3.) The Sensory nucleus of the 5th: ipsilateral alteration of pain and temperature on the face in the distribution of the 5th cranial nerve (this nucleus is a long vertical structure that extends in the lateral aspect of the pons down into the medulla).
- 4.) The Sympathetic pathway: ipsilateral horner’s syndrome, that is partial ptosis and a small pupil (miosis).
Why would a neurologist send a patient to get an ECG?
- Stroke risk: Atrial fibrillation is one of the largest risk factors for stroke.
- - The increased and unco-ordinated contractions of the atria can create stagnant flow in the auricles where clots can form.
- - These can embolise and travel out and can lodge in the brainstem causing an ischaemic stroke.
Malcolm Parker; 64 YOA and heavy smoker
- onset of nausea and headache
- Paramedic sees right side face paralysis (upper and lower) and
- right eye is deviated medially while left eye appeared normal
5 days later shows increased tone and brisk tendon reflex in left limb
Determine site and nature of neuro signs using a diagram
What deficits might be discovered if sensation in limbs and face were examined?
- This is likely a medial pons lesion on the right side for these reasons;
- - latitudinally, the nature of his eye defect seems to be due to loss of his lateral rectus muscle. This means that relative tone of medial muscles controlling the eye are higher and there is medial deviation. This is strongly suggestive of an infarct in the abducens nucleus
- - loss of voluntary movement of right face muscles of upper and lower face suggests an ipsilateral LMN defect. The facial nerve nuclei (although slightly lateral) has tracts which travel medially and would also be affected by a medial infarct
- - Consistent with the site of this infarct are the UMN symptoms on the contralateral (left side); i.e. increased tone, and heightened tendon reflex
- - Nausea etc from increase ICP or pain
- Other brainstem nuclei in this region include;
- - Trigeminal, Facial and Vestibulocochlear (but this one is bilaterally innervated so no auditory loss)
- - The trigeminal motor and sensory nuclei are more out of the way (more lateral and superior); so not sure if affected and depends on size of infarct but if so; cutaneous sensation (and corneal reflex) on the ipsilateral side, and loss of jaw/chewing muscles (so face droop)
- - Also running medial is the medial lemniscus pathway for discriminative sensation which would be lost for the limbs on the left side
List the tests you might perform on to assess his hearing and what results you might expect if the patient did in fact have “glue ear”.
- Rinne: air vs. bone conductance of one ear
- - bone conduction is louder with conductive defect.
- Weber: if conductive weber test localises to the affected side.
- Tympanometry: is useful for diagnosing middle ear effusion.
- - an examination used to test the condition of the middle ear and mobility of the eardrum (tympanic membrane) and the conduction bones by creating variations of air pressure in the ear canal
With the aid of an otoscope
the tympanic membrane can be examined for signs of dilated vessels, bulging and suppuration which are associated with glue ear.
It is not usually worthwhile doing lab cultures to identify the cause of the infection because bacteria are usually not present in the fluid. They tend to form a biofilm within the middle ear.
What would you like to do?
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