Neuro Flashcards

Question

Stroke Diagnosis

Answer 1

Collections of signs and symptoms resulting from strokes in different regions of the brain/CNS

Answer 2

medial & superior frontal and parietal lobes corpus callosum basal ganglia

Answer 3

1. Contralateral weakness Legs > Arm/Face Motor homuniculus distribution 2. Contralateral Sensory deficits 3. Abulia Absence of willpower or the inability to act decisively 4. Speech Disturbance Transcortical motor aphasia: non-fluent, difficulty intiating speech Transcortical Mixed aphasia: speaking + comprehension impairment 5. Urinary Incontinence Voluntary bladder control areas affected 6. Ipsilateral ataxia + contralateral leg weakness 7. Bilateral ACA involvement Bilateral leg weakness Frontal disinhibition -Primitive reflexes return e.g grasping, suck reflexes -Personality changes

Answer 4

Temporal Lobe Anterolateral Frontal lobe Parietal Lobe

Answer 5

*No facial Involvement/speech disturbance*

Answer 6

Occipital lobe Inferior Temporal Lobe Thalamus Midbrain

Answer 7

Extra-Axial Haemorrhage: Bleeding that occurs within the skull but outside the brain tissue Epidural Subdural Subarachnoid Intra Axial Haemorrhage (Inside Brain tissue) Intracerebral Intraventricular

Answer 8

Bleeding between the skull and the dura mater Source of blood is often arterial (Middle meningeal artery) Causes: Skull fractures (70-95%). Head trauma includes: motor vehicle accidnet, fault, assault

Answer 9

Altered consciouscness Headache Vomiting Confusion/seizures Aphagia

Answer 10

Bleeding between the dura mater and subarachoid membrane Source of blood often tearing of the bridging veins

Answer 11

Coma (50%) Lucid interval -> Progressive neuro decline -> Coma

Answer 12

Haemorrhage within arachnoid space Source of blood from rupturing of aneurysm (cerebral artery) Causes: Rupture of sacular aneurysm -> subarachnoid haemorrhage

Answer 13

Sudden severe headache Loss of consciousness/Seizure Nausea/Vomiting Meningismus

Answer 14

Lobar haemorrhage Thalamic haemorrhage Pontine hameorrhage Cerebellar haemorrhage

Answer 15

Second most common cause of stroke Aetiology: Hypertension Embolism Brain tumour Bleeding Disorder Drugs Clinical Manifestations Neurological signs and symptoms (Depending on area) Headache Nausea/Vomiting Decreased loss of consciousness

Answer 16

Bleeding confined to the ventricular system of the brain Most often occurs as a secondary phenomenon when intracerebral haemorrhage ruptures or when subarachnoid haemorrhage extends to the ventricles

Answer 17

CT scan MRI Angiography

Answer 18

Drugs -for hypertension -to relieve intracranial pressure Surgery -Craniotomy: part of skull removed to drain blood and relieve pressure -Stereotactic aspiration: aspirate off blood and relieve pressure

Answer 19

Chronic and progressive autoimmune demyelinating disease of the nerve cells in the brain, spinal cord characterised by various neurological disorders Cell-mediated (Type IV) hypersensitivity reaction

Answer 20

Type IV hypersensitivity 1.T cell crosses blood brain barrier. Becomes activated by myelin 2.T cell changes blood brain barrier, expressing more receptors for immune cells to cross blood brain barrier 3. Cytokines (IL-1, IL-6, TNF - alpha, INF- gamma) released by T cells dilates blood vessels (allowing more cells to get in) and directly damages oligodendrocytes 4. Attracts B cells which produce antibodies that mark myelin sheath proteins, And macrophages which use those antibody markers to engulf and destroy oligodendrocytes. 5. Without oligodendrocytes, no myelin covers the neurons leaving sclera 6. Attacks happen in bouts Early on: remyelination occurs Overtime: Irreversible

Answer 21

Vary, depends on location of plaques Affects 20-40 years old Worsen over weeks;linger for months Charcot's neurological triad Also (see pic)

Answer 22

Autoimmine demyelinating disorder that leads to progressive paralysis Most common cause of acute flaccid, neuromuscular paralysis worldwide

Answer 23

Neurodegenerative condition resulting from loss of dopaminergic neurons in the brain, characterised by associated motor symptoms

Answer 24

Basal Ganglia

Answer 25

Direct facilitates movement Indirect terminates movement

Answer 26

Thought that the degeberation of neurons in substantia nigra pars compacta is due to the accumulation of Alpha's Nuclein (protein involved in regulation of the synaptic vesicles and release of neurotransmitters) Close Link to Lewys Body dementia

Answer 27

Appear when 50% of neurons have been lost 1.Bradykinesia 2.Rigidity (muscle stiffening): Cog wheel rigidity, Lead Pipe rigidity 3.Hypomimia - Expressionless Face 4.Tremors (Pill Rolling Tremor) - Mostly resting 5.Gait Disturbance - Shuffling gait. Also at an increased risk of falls = Collectively these symtpoms are known as Parkinsonism (80% of Parkinsin's Disease). Others include -Drug induced -Multi-system atrophy -Progressive Supranuclear Palsy -Normal Pressure Hydrocephalus Other symptoms include: 6. Autonomic disturbance: Hypersalivation, constipation/incontinence 7. Cognitive Impairment

Answer 28

Most cases are idiopathic 1.Genetics: -2x risk in 1st degree relatives -10-15% of cases are familial: Autosomal Dominant, Autosomal recessive 2. Environmental -Rural living -Exposure to industrial chemicals -Infections: Encephalitis 3. Age- mean age 60 -5-15% before 40 -1% of people over 60 4. Males : Females (1.5:1)

Answer 29

Clinical Diagnosis Movement Disorder Society Parkinson's Disease Criteria: 1.Bradykinesia + Resting Tremor/Rigidity + 2. 2 Supportive Criteria + 3. No exclusion or red flag criteria Dat Scan: Radioactive Isotope + SPECT scan

Answer 30

1. Medication 2. Deep Brain stimulation: -Pulse generator placed under skin -Electrodes placed in vicinity of basal ganglia

Answer 31

Initially medication may treat symptoms well however as time goes on there is less of an effect and the on/off phenomenon inevitably appears with the use of levodopa. Overtime the window for controlled symtpoms known as the on phase gets tighter. While off is a state of rigidity and uncontrolled symptoms. The switch from on to off and vice versa can happen quickly. This kinesias are involuntary movements that are a side effect that can occur when patients flip between on and off known as diphasic dyskinesia. It can also occur following levadopa medication giving peak dopamine levels known as peak dose dyskinesia.

Answer 32

Huntington disease, or HD, is a rare neurodegenerative disease that involves a repeated sequence of DNA that causes an abnormal protein to form, leading to abnormal movements and cognitive problems. Autosomal Dominant genetic disorder

Answer 33

Mutation in a single gene called huntingtin. This is a dominant mutation. Thus if 1 parent has the disease, their child has a 50% chance of developing it too. The huntingtin gene contains a DNA sequence that consists of nucleotides (CAG) in repitition - known as trinucleotide repeat. When the gene is mutated an excess no of repeats can occur and a mutated form of huntington protein is created. The higher the noof repeats the greater the risk of disease, and all people with 36 or more repeats in the huntingtin gene will develop Huntington's disease. Mutated Huntingtin proteins ahve a tendency to group together, forming clusters within neuros that are not easily removed by brai enzymes. Accumulation in the brain is associated with increased neurodegeneration.

Answer 34

Progressive neurodegenerative disease characterised by cognitive decline that causes impairment in daily functioning

Answer 35

1.Alzheimer's Disease 2.Vascular dementia 3.Dementia with Lewy Bodies 4.Frontotemporal dementia

Answer 36

Symptoms get progressively worse over time Cognitive Decline >=1 of: 1.Memory 2.Executive Function 3.Language 4.Attention 5.Visuospatial function

Answer 37

70% of dementia Caused due to the accumulation of insoluble proteins in the brain: beta amyloid plaques: extracellular hyperphosphorylated Tau protein (normally involved in microtubules): intracellular neurofibrillary tangles Beta amyloid may be found in non-dementia brains -Increased quantity in Alzheimer's -Mostly hippocampus , parietal, temporal lobes

Answer 38

1.Short term memory loss 2.Difficulty finding words 3.Disorientation 4.Poor insight

Answer 39

Involves reduced blood flow to neurons giving ischaemia and cell death 1.Multi Infarct Dementia Series of small strokes that together cause symptoms 2. Subcortical dementia Small penetrating arteries affected (small vessel disease) 3. Stroke related dementia 30% of ischaemic strokes Function decreases in a step-wise manner

Answer 40

1.Smoking 2.Diabetes 3.AF 4.Dyslipidaemia 5.Hypertension 6.Age Risk doubles every 5 years

Answer 41

1.Smoking Diabetes

Answer 42

Impairment in : Planning Organising Judgement occur early on

Answer 43

10% Lewy Bodies: Spherical, intracellular deposits formed from alpha synuclein + ubiquitin Primary abnormality in Parkinson's Disease dementia

Answer 44

Core symptoms 1. Flucuating cognition 2. Visual hallucinations (2/3) 3. Parkinsonian Features: Bradykinesia, rigidity, falls, autonomic dysregulation(orthostatic hypotension, incontinence/constipation) Suggestive symptoms 1.REM sleep disturbances 2.Sensitivity to antipyschotics

Answer 45

Second most common dementia in under 65s: mean age of onset 53 Involved proteins: 1.TDP 43 (DNA binding protein) 2.Tau protein (microtubule protein) Types: 1.Behavioural variant (BvFTD) *Pick's disease* Most common Personality/behavioural changes early -Disinhibition/social withdrawal Pick Bodies: Spherical intracellular collections of tau fibrils 2. Semantic Variant Difficulty finding correct words impaired comprehension Fluent Aphasia 3.Non fluent variant Progressively more hesitant speech =2 + 3 are primary progressive aphasia

Answer 46

1. Age is the largest risk factor -Age 65 = 2% -Age 85 = 40% 2. Genetics: -10-30% increased risk in 1st degree relative -Early Onset dementia (<65years): Trisomy 21, 5% of alzheimer's overall (and majority of early onset) has autosomal dominant inheritance with near complete penetrance Early genes: Late genes: 1. APP Ch21 1. Apolipoprotein E: E4 variant (1 allele = 50%)(2 allele = 90%) 2. Presenilin 1 Ch14 3. Presenilin 2 Ch 1 3. Gender: F>M 4. Cognitive Reserve Social isolation Left education early Low job complexity 5. Vascular Risk Factors

Answer 47

Post mortem brain biopsy traditionally only mode of confirmation -Rarely done on living people -PET scan can demonstrate histological features of Alzheimer's 1.Clinical History + Physical Exam 2.Mental State Examination: MMSE/MOCA 3.Lab investigations: Blood typically normal Vitamin B12/Folate Thyroid Function Tests Electrolyte Panels Infection (e.g Lyme's disease + neurosyphilis) 4. CT head Exclusion of chronic intracranial bleed or normal pressure hydrocephalus Cerebral atrophy 5. Genetic Testing

Answer 48

No cure currently 1 year mortality 30-40%. 5 year mortality 65% 1.Medication Cholinesterase inhibitors: donepezil, galantamine, rivastigmine) NMDA antagonists: memantine = slow cognitive decline but effect on survival unclear 2. Risk Reduction (Especially vascular) 3. Behavioural + Environmental support Maintain familiarity Monitor personal comfort Attention redirection 4.Mental Health Support 5.Aerobic exercise

Answer 49

Meningitis (bacterial, viral and fungal) Encephalitis

Answer 50

Inflammation of the leptomeninges (arachnoid and pia maters)

Answer 51

Meningitis : Inflammation of the leptomeninges + Encephalitis : Inflammation of the brain

Answer 52

Inflammation triggered by: 1.Autoimmune disease: Lupus 2.Adverse reaction to medication: Intrathecal therapy (injected directly into CSF) 3.Infection (most common): Neisseria meningitidis, Herpes simplex 2 routes an infection takes to reach CSF and leptomeninges 1.Direct spread (Pathogen gets inside skull/spinal column and penetrates the meninges and eventually CSF): Through overlying skin Up through nose Anatomical defect: congenital (spina bifida). acquired (skull fracture) 2. Haemotogenous spread Through binding to surface receptors/areas of damage/vulnerable spots Pathogen recognised by CSF and produces more white blood cell. 1ul Greater than 5 WBC -> meningitis

Answer 53

Stiif and Painful Neck Fever Altered Mental Status Headache Photophobia & Phonophobia Malaise & Fatigue Nausea/Vomiting Anorexia Skin Rash Cold Extremities Papilledema: Swelling of optic nerve due to increased ICP Seizures Cranial Nerve Palsies

Answer 54

Kernig's sign Brudzinski's sign Lumbar puncture (needle between L3 & L4 takes CSF): Measure pressure, analyse WBC, protein & glucose PCR: Look for HIV, Enterovirus, HSV, TB Western Blot: Borrelia burgdorferi Thin Blood Smear: Malaria

Answer 55

Condition involving inflammation of the brain parenchyma May be due to a variety of causes

Answer 56

Other Features: Meningitis signs and symptoms Nuchal rigidity ("Stiff neck") Brudzinski's sign Kernig's sign

Answer 57

Most ubiquitus headache and is the most common reason why OTC analgesics are purchased Location: Bilateral Character: Pressure or toghtness which waxes and wanes Duration: Variable Associated symptoms: None

Answer 58

A disorder of recurrent attack Location: Unilateral (70%) Character: gradual onset, crescendo pattern, moderate-severe intensity Duration: 4-72 hours Associated symptoms: nausea, vomiting, photophobia, phonophobia, aura

Answer 59

Form of trigeminal autonomic cephalgia 0.1% of population "Suicide headache" - excruciating Unilateral -Eye/Temple <4hr duration Sweating, tearing, hypermia, ptosis, rhinorrhea, restlessness Cyclical/Consistent timing Precipitated by alcohol More common in men and smokers Episodic: episodes present on 7-365 days of the year with at least 1 month complete remission Chronic: pain ongoing beyond 1 year, less than 1 month complete remission Treatment : Acute: 1. Oxygen therapy 2. Triptans Prevention: 1. Verapamil (CCB) 2. Lithium 3. Topiramate 4. Deep Brain/Occipital Nerve stimulation

Answer 60

Neurological condition involving recurrent episodes of facial pain

Answer 61

Clinical diagnosis MRI to rule out secondary causes (lesions)

Answer 62

1st line therapies: Carbamazepine Oxcarbazepine

Answer 63

Transient occurence of signs and symptoms due to abnormally excessive or synchronous neuronal activity within the brain

Answer 64

1st: where the seizure originated in the brain Generalised: Involve both hemispheres of the brain Focal: Originate from an area on one hemisphere *If seizures begin on one hemisphere and then involve both sides, they are known as focal to bilateral seizures 2nd: whether or not patient keeps their awareness during the seizure Generalised seizures are automatically considered to affect awareness, only applies to focal seizures Focal Aware = Simple Focal Unaware = Complex 3rd: Motor/Non-motor involvement during the seizure Generalised seizures may feature stiffening and jerking Focal Seizures can have movements twitching, jerking and stiffening + automatic movements like licking lips or rubbing hands Focal seizures: one group of muscles may be affected but abnormal movement can spread to other muscle groups . Due to abnormal neuronal activity of brain also moving to a diff area - *JACKSONIAN MARCH*. Generalised non-motor seizures are known as absent seizures where individuals will rpimarily have changes in awareness and stay Focal non-motor seizures typically have other symptoms that happen first (aura) e.g changes in emotion/sexperiences/thinking

Answer 65

>5 mins seizure duration Medical emergency Benzodiazepine, phenytoin, phenobarbital

Answer 66

Following a seizure there is a postictal phase Lasts min-hours Confusion Tiredness Headache Speech difficulty 10% pyschosis Amnesia

Answer 67

4. Follow up - specialist clinic Antiepileptic drugs: valproate, lamotrigine, levetiracetam

Answer 68

Neuron located within brain/brainstem Axon travels down spinal cord Innervates alpha & gamma motor neurons in ventral horn

Answer 69

Alpha & Gamma motor neurons located in the ventral horn of the spinal cord Axon travels to periphery to innervate muscle

Answer 70

Acquired autoimmune condition involving neuromuscular blockade and subsequent muscle weakness It is a type II hypersensitivity reaction Most common neuromuscular junction disorder affecting skeletal muscles

Answer 71

Fluctuating muscle weakness and fatigue of heavilt used muscle groups -Worsens with activity and improves with rest -Weakness worse in the afternoon hours -Weakness involves muscles of the eyes, extremities and throat Extraocular Muscle Weakness -Ptosis, Diplopia (often none in morning): Unilater or bilateral -Often intial finding -Most common symptom Ocular MG -> Generalised MG Continuing see pic

Answer 72

Autoantibodies produced against acetylcholine receptors & other muscle components

Answer 73

Lamber-Eaton Syndrome (Paraneoplastic) Guillain Barre Syndrome Motor Neuron Disease

Answer 74

Cluster of major degenerative diseases Characterised by selective loss of neurons in motor cortex, cranial nerve nuclei and anterior horn cells Upper and lower motor neurones are affected, but there’s NO sensory loss or sphincter disturbance – distinguishes from MS and polyneuropathies Never affects eye movements – distinguishes from myasthenia Relentless and unexplained destruction of upper motor neurones and anterior horn cells Most will die in 3yrs from respiratory failure due to bulbar palsy and pneumonia

Answer 75

Most are sporadic with no family history Rare familial cases Mutations in the free radical scavenging enzyme copper/zinc superoxide dismutase (SOD-1) Suggests that oxidative stress and free radicals play a role in destruction of motor neurones

Answer 76

4 clinical patterns: ALS/amyotrophic lateral sclerosis – 50% Loss of motor neurons in motor cortex AND anterior horn of cord Weakness + UMN signs e.g. upgoing planters + LMN wasting/fasciculation Worse prognosis if – bulbar onset, older, reduced FVC Split hand sign- thumb’s side of the hand seems to separate from the rest owing to excessive wasting around it Progressive bulbar palsy – 10% Only affects cranial nerves IX-XII LMN lesion of the tongue and muscles of talking and swallowing – Flaccid, fasciculating tongue Jaw jerk is normal or absent Speech is quiet, hoarse or nasal Progressive muscular atrophy – 10% Anterior horn cell lesion only No UMN signs Affects distal muscle groups before proximal Primary lateral sclerosis Loss of Betz cells in motor cortex Mainly UMN signs Marked spastic leg weakness and pseudobulbar palsy No cognitive decline Suspect MND in >40yrs Stumbling spastic gait, foot-drop ± proximal myopathy Weak grip and shoulder abduction UMN signs – spasticity, brisk reflexes, upgoing plantars LMN signs – wasting, fasciculation of tongue, abdomen, back, thigh

Answer 77

Brain/spinal cord MRI excludes structural causes Lumbar puncture excludes inflammatory ones

Answer 78

Antiglutamatergic drugs – riluzole Drooling – propantehline, amitriptyline Dysphagia – blend food, NG tube Spasticity – baclofen, diazepam Joint pains and distress – follow analgesic ladder Respiratory failure – non-invasive ventilation at home may allow palliation

Answer 79

Metastatic spinal cord compression (MSCC) is an oncological emergency that describes when tumours (usually having spread from another part of the body) grow in the spinal column and compress the spinal cord. L1-L2 anything below is cauda equina syndrome

Answer 80

Spinal metastases -Lung -breast -myeloma -lymphoma -prostate

Answer 81

Cauda equina syndrome is a condition caused by damage to the bundle of peripheral nerves protruding from the bottom of the spinal cord, called the cauda equina.

Answer 82

Reversible loos of consciousness due to inadequate blood flow to the brain -Fast onset -Short duration -Spontaneous recovery

Answer 83

Blacking out. Feeling lightheaded. Falling for no reason. Feeling dizzy. Feeling drowsy or groggy. Fainting, especially after eating or exercising. Feeling unsteady or weak when standing. Changes in vision, such as seeing spots or having tunnel vision. Headaches.

Answer 84

Medicines for syncope include: Midodrine. Fludrocortisone

Answer 85

* Carpal tunnel syndrome * ‘Wrist drop’ * ‘Claw hand’ * ‘Foot drop’

Answer 86

Cindition involving impingement (or entrapment) of the median nerve in the wrist Most common entrapment neuropathy

Answer 87

Median nerve becomes compressed in the carpal tunnel due nto bone growth and/or soft tissue proliferation

Answer 88

The patient is unable to lift the front of the foot up due to weakness or paralysis of the tibialisi anterior muscle which lifts the foot up

Answer 89

When the patient with foot drop walks, the foot slaps down onto the floor Steppage gait means that the patient slaps his foot down onto the floor because the foot drops, and his gait will show that he is raising the thigh up in an exagerrated fashion while walking

Answer 90

Usually results from an injury to the common peroneal nerve. This nerve is susceptible to injury at any point of its course Conditions causing foot drop: 1.L4-L5 disc herniation: Herniated disc compressing the L5 nerve root may cause foot drop 2.Lumbrosacral plexus injury can occur from a pelvic fracture with displacement of the sacriliac joint 3.Hip/Knee dislocation 4.Neglected compartment syndrome Systemic causes: diabetes, ischaemia, inflammatory conditions

Answer 91

Usually results from an injury to the common peroneal nerve. This nerve is susceptible to injury at any point of its course Conditions causing foot drop: 1.L4-L5 disc herniation: Herniated disc compressing the L5 nerve root may cause foot drop 2.Lumbrosacral plexus injury can occur from a pelvic fracture with displacement of the sacriliac joint 3.Hip/Knee dislocation 4.Neglected compartment syndrome Systemic causes: diabetes, ischaemia, inflammatory conditions

Answer 92

Non operative treatment: Observation Therapy Stretching Range of motion of the ankle AFO bracing Surgery: Nerve repair/grafting if there is laceration of the nerve If the injury is chronic, you will do a posterior tibial tendon transfer to the lateral cuniform, in addition to achilles tendon lengthening Split posterior tibial tendon transfer

Answer 93

characterisitic deformity of a radial nerve lesion The wrist remians in the palamr flexion due to weakness of the dorsiflexions. It is seen in radial nerve palsy

Answer 94

Radial nerve = big Trauma -Shoulder dislocation -Fractures (Humerus, supracondylar, monteggia) Compression -Saturday Night Palsy -Crutch Palsy

Answer 95

Tendon transfer operation

Answer 96

Ulnar nerve palsy Claw hand is a condition that causes curved or bent fingers

Answer 97

Causes may include: Congenital abnormality Genetic diseases, such as from Charcot-Marie-Tooth disease Nerve damage in the arm Scarring after a severe burn of the hand or forearm Rare infections, such as leprosy

Answer 98

Medical History Physical Examination Electromyography

Answer 99

Physical therapy Surgery

Answer 100

Atherosclerotic emboli in the eye Heart disease, especially irregular heartbeat Alcohol abuse Cocaine use Diabetes Family history of stroke High blood pressure High cholesterol Increasing age Smoking (people who smoke one pack a day double their risk for a stroke) Amaurosis fugax can also occur because of other disorders such as:

Answer 101

Amaurosis fugax can also occur because of other disorders such as: Other eye problems, such as inflammation of the optic nerve (optic neuritis) Blood vessel disease called polyarteritis nodosa Migraine headaches Brain tumor Head injury Multiple sclerosis (MS), inflammation of the nerves due to the body's immune cells attacking the nervous system Systemic lupus erythematosus, an autoimmune disease in which the body's immune cells attack healthy tissue throughout the body

Answer 102

Rare Autoimmune Neuromuscular junction disorder -> presynaptic neurons This is due to a decreased Ach release and therefore reduced contraction Improves temporarily after repeated use

Answer 103

Small Cell Lung Cancer Also associated with: Hashimoto's thyroiditis Diabetes Mellitus type 1

Answer 104

Autoimmune response against voltage-gated Ca2+ chnnels Affects somatic and parasympathetic nervous system Type II hypersensitivity reaction: antibody production against its own protein Antibodies bind and block most Ca2+ channels: Low Ca2+ with neuron -> no Ach release -> no muscle contraction With repeated stimulation -> enough Ca2+ gets through -> Ach release -> muscle contraction

Answer 105

Symmetrical weakness of proximal muscles -Shoulders, hips and thighs -Difficulty climbing stairs and standig up Reduced reflexes Warming-up phenomenon: weakness is relieved temporarily after repeated use Advanced stages: weakness in the respiratory muscles -> respiratory failure Most have autonomic symptoms: dry mouth, constipation, blurred vision, urinary problems, fainting

Answer 106

Condition that results from damage (resection) to one half of the spinal cord on either side This hemisection causes damage of the spinal cord tracts This syndrome results in weakness or paralysis (hemiparaplegia) on one side of the body and a loss of sensation (hemianesthesia) on the opposite side Damages: Descending Corticospinal tracts Ascending dorsal column tracts Spinothalamic tracts

Answer 107

A sensory stimuli passes through three neurons The lateral branch of the 1st order neuron carries info to the dorsal root The second order neuron crosses over to the opposite side of the spinal cord Third order neuron located in the ventral posterior region of the thalamus to the sensory cortex of the brain

Answer 108

Group of hereditary, progressive neurlogical disorders of the PNS, impaired sensory/motor function Inherited Worsen overtime

Answer 109

Defective proteins in myelin sheath or axon -> signals fail to reach target tissues: sensory & motor

Answer 110

CMT1: Autosomal dominant Mutations in PMP22 & MPZ: Encode proteins part of myelin sheath (made by schwann cells) Slows down electrical impulses CMT2: Autosomal dominant Mutations in MFN2: Encodes Mitofusin-2 (expressed in neuronal mitochondria) When defective: mitochondrial function (-> neuronal death)-> disrupted in both CMT1 & CMT2, motor neurons are affected, muscles begin to atrophy ("use it or lose it"). When sensory nerves are affected the feet and toes are first affected

Answer 111

presence of risk factors imbalance of lower limb strength lower extremity musculotendinous contractures delayed motor milestones

Answer 112

stage 1: ambulatory 1ST LINE – corticosteroids stage 2: non-ambulant 1ST LINE – supportive therapies to maintain activities of daily living stage 3: ventilator-supported 1ST LINE – inspiratory and expiratory respiratory muscle assistance

Answer 113

A mental state of low mood

Answer 114

*Multifactorial* 1. Genetics High concordance rates in twins Family History 2. Environmental Stressful life events Childhood abuse Substance abuse/medical conditions Diasthesis-Stress model: See pic

Answer 115

*Not entirely understood* 1. Monoamine theory: lack of monoamine neurotransmitters (serotonin, dopamine, norepinephrine) Decrease in serotonin is not equal to depression in healthy individuals Anti-depressants restore levels quickly, but take weeks to improve clinical symptoms 2. Hypothalamic-Pituitary Axis Disturbance Increase Cortisol, decrease dexamethasone suppression Link to growth + thyroid hormones 3. Immune system Excessive cytokine release Improvement of symptoms with NSAIDs Close link between asthma and depression

Answer 116

1. Lifetime risk ~ 12% 2. Female : Male 2:1 Different pyschosocial pressures Hormonal Diff 3. Mean onset ~ 40 years Becoming increasingly common in younger ages

Answer 117

*Combinations more effective* 1.Lifestyle 2.Pyschotherapy *Favoured in U18s: CBT, interpersonal therapy 3.Medication: SSRI: Setraline, citalopram, fluoxetine SNRI: Duloxetine, venlafaxine Atypical: mitrazapine TCA (amitriptyline) MAOI (selegiline) Vit D COX-2 inhibitors (Celecoxib) 4. Electroconvulsive therapy Electrically Induced Seizure 50% effective in treatment resistant MDD. 50% relapse in 12 months

Answer 118

Primary: Tumour in the brain that arose from associated tissue Secondary: Tumour in the brain that metastasised there from elsewhere

Answer 119

Glioma Meningioma Pituitary adenoma

Answer 120

Progressive focal neurological deficit: Symptoms depend on location (frontal lobe -> personality change etc). Speed of deterioration is proportional to growth of tumour Raised intracranial perssure: Headaches (worse on cough/leaning forward), vomiting and papilloedema. Epilepsy: Focal or generalised General cancer symptoms: Weight loss, malaise, anaemia etc False localising signs: Raised ICP or the presence of a tumour can cause healthy structures to affect adjacent ones. E.g., Downward displacement of temporal lobe -> III or VI CN palsy

Answer 121

Progressive focal neurological deficit: Mass effect of the tumour and oedema -> impact functionality of site associated with tumour. Can destroy tissue -> rapid deterioration Raised ICP: As tumour grows -> downward displacement of the brain -> pressure on the brainstem (drowsiness) -> respiratory depression -> coma -> death. False localising signs possible (see left) Epilepsy: Tumour creates unusual electrical impulses -> seizures

Answer 122

Derived from the skull itself, or adjacent structures. 95% of primary tumours are Gliomas or Meningiomas (others include neurofibromas and lymphomas)

Answer 123

Metastases from: Bronchus, Breast, Kidney, Thyroid, Stomach, Prostate

Answer 124

About 10% of all neoplasms

Answer 125

CT and MRI. Positron Emission Tomography to find occult metastasis

Answer 126

Surgery: Exploration, removal or biopsy (meningiomas can be fully removed without incident) Radiotherapy: Gliomas and radiosensitive metastases Medical: Cerebral oedema can be reduced with corticosteroids. Epilepsy treated with anticonvulsants.

Answer 127

Neuropathy of the peripheral nerves

Answer 128

3 types: autonomic, motor and sensory

Answer 129

Can be asymptomatic. Diabetes: Long history of paresthesia (glove stocking), pain, weakness and wasting, autonomic symptoms; incontinence, sexual dysfunction). Usually present as foot ulcers (constant damage due to paresthesia)

Answer 130

Diabetes: Hyperglycaemia damages 3 cell types; retinal endothelium, mesangial cells in glomeruli and schwann cells in perpheral nerves (these cell types cannot regulate their glucose well, so constant hyperglycaemia causes excessive oxidation -> damage)

Answer 131

Acute: Guillain barre Chonic: Diabetes, alcohol

Answer 132

Nerve conduction studies. FBC. Diabetes: As in DM

Answer 133

Diabetic control. Amitriptyline for neuropathic pain.