Neurology Flashcards
1
Q
Which diseases are stroke mimics?
A
Hypoglycaemia, labyrinth disorders, Migranious aura Typical and atypical, Mass lesios, postictal weakness simple partial sizures funcional hemiparesis
2
Q
How is TIA managed In primary care?
A
Assess risk of stroke or TIA in next 7 days in guidance and refere to specialist if needed
3
Q
What contributes to high risk of recurrent stroke or TIA?
A
ABCDsquared above 60 High BP clincial features duration diabetes AF more than one week or on anticoagulant
4
Q
What to do in low risk TIA patient?
A
Refer from assessment, statin antiplatelet, treat BP no driving till seen specialist
5
Q
What layer are the somites made of?
A
Mesoderm
6
Q
What are derived from somites?
A
dermatomes and myotomes (skeletal only)
7
Q
What are branchial arches?
A
Bumps belwo the head around the neck they are a feature of vertibrates
8
Q
Which area are sympathetic nerves derived from?
A
T1-L2
9
Q
Which cranial nerves are carying autonomic nerves/
A
3,7,9,10 1973
10
Q
What makes up peripheral nervous system?
A
spinal cord C8 T12 L5 S5 some (1)coygeal ones, then the ones from the brain cranial nerves somatic branchial autonomic and special
11
Q
Where are the Thoracic dermotomes?
A
They are from the sinal level at the back to slightly lower at the front they run from above the ribs down to the suprapubic area T1 gos down the inside of the outer arm
12
Q
Where is the foregut pain felt/
A
In T5 to T9 dermatomes in epigastrium
13
Q
Where does hindgut pain feld?
A
In T12 region suprapubically
14
Q
Where does the spinal cord end?
A
At around L1
15
Q
What is important about spinal cord deficites level?
A
Spinal cord level is where the bodies of the cells are in the cord where as the vertebral level is where they ender the spinal column
16
Q
Where does the splanchnic nerves come from?
A
They come from the sympathetic chain
17
Q
What is the corticospinal tract?
A
Motor tract from the cortex through internal capsule in thalamus, to thepons and medulla where 85% cross to the contralateral side to the lateral corticospinal tract 5% are on ipsilateral spinal tract the other 1-0 are in the ipsilateral anteria corticospinal tract
18
Q
What is significance of decusation of the corticospinal tract?
A
if you hafe brain or stem injury it will affect contralateral side otherwise it affectsthe same side if below the medulla
19
Q
What does anterior corticospinal tract do?
A
Muscles of the trunk
20
Q
What happens with anterior decussation?
A
Happens in the thoracic cord not the pyramids
21
Q
What is in the ventral horn of the spinal cord?
A
the motor nerves
22
Q
What are in the dorsal horm of spinal cord?
A
The sensory nerves
23
Q
What happens with thoracic spinal hemisection in corticospinal?
A
Loss of motor to the same side for the limb but opposite for the trunk
24
Q
What doe the dorsal columns carry?
A
They carry touch vibration concious muscle/joint sense
25
What is in the fasciculus gracilis?
The leg sensation
26
What is in the fasiculus cuneatus?
the arm sensation
27
Where is the gracilis ?
In the middle
28
Where do the dorsal columns cross?
up the spinal cord on same side and then synapse in medull and cross then up to thalamus then to the cortex
29
How many neurones are in the dorasal columns pathway?
3 limb to medulla, decussation then new one tothalamus then corte
30
What are in the spinocerebellar pathways?
joint and muscle non concious sense anterior and posterior divisions
31
What is the pathway of the spinocerebellar/
Posterior decussates later anterior as soon as joins
32
What is carried in the spinothalamic tract?
Pain and extreme temperature and it decussates a few segments above where enters
33
What is Brown-Sequard syndrome?
A lesion at right level T10 vertebral elvel T6 ish will lose all normal sensations on the same side of body as dorsal columns cross in medulla lose pain and temperature on thecontralateral side a few segments down and also total loss of all sensation in ipsilateral side, paralysis on same side from injury down
34
What might happen in high spinal cord injury?
The tunk musscles on other side will get damaged.
35
Where is a lumbar puncture done and why?
In the lumber spine because the spinal cord takes up less space so its easier to not dammage the cord
36
What is difference between lumbar puncture and epiduuural?
The epidural is done with a blund needle outsided the dura whereas lumbar puncture should go into the dura
37
What is in the olfactory nerve?
85% on same side of brain and it is special sense not through the thalamus
38
What is the optic nerve?
Special sense 50% cross over when testing look at light then neuronal
39
What is the oculomotor
somatic and autonimic motor, lense and pupil control and the eye movements recti but nod lateral
40
What does the trochlea nerve do?
somatic motor tor superior oblique down and out if have occularmotor palsy
41
What does abducents nerve do?
Lateral recuts somatic motor
42
What does trigeminal do?
Branchial motor and sensory somatic bilateral motor to face and contralateral sensory to face also muscles of mastication nasal cavity and sinuses
43
What is in the facial nerve?
Motors autonomic branchial ans special sensory. does motor to bilateral forehead motor to contralateral rest of cace and sensory to the tongue the anterior
44
What are the common ways blood supply to the brain is interrupted?
85% embolic, 10% haemorrhagic and 5% have rarer causes
45
How can emboli in the brain form?
Infarction of endocardium and diseased valves, or in atherosclerotic events in great vessels common carotid internal carotid or vertebral arteries
46
Which blood vessels supply the basal ganglia?
The middle cerebral arteries, lenticular nucleus
47
What can happen if internal capsule ishaemmoraged?
the cotex function is blocked as well
48
What does the secondary auditory area?
the library of sounds that we know so if dammaged can hear things but not make sense of them
49
What parts of the body ares are affected in anterior infarction?
lower limb sensory and motor deficit
50
What areas of the body are affected in the posterior artery infarction/
Non as doesnt supple the motor homunculus
51
What is an extradural haemmorage?
On outside the dura
52
What is subdural haemorrage?
one between the dura and the arachnoid mater
53
What doe meningeal blood vessels do?
They run between the skull and dura and supply skull and dura with blood
54
Where are the veins of the brain?
Between the durathe periosteum and meningeal
55
What are bridging veins?
Veins that cross the subdural space between the
56
Which vessels are deep to the pia?
None
57
What can cause extradural haemorrhage?
Damage to the meningeal artery from trauma fractured skull, rise in intercranial pressure can cause coning and death
58
What stops the bleed of an extradural haemorrage?
When pressure in skull is the same as inside the vessels
59
What happens in the extradural haemorrage?
The blood builds up and squashes the brain causing a haematoma under the bone contained by a sutre
60
What causes a subdural haemorrhage?
smaller brains, alcoholicas dementia and babies with acceleration change, bridging vessels broken days or weeks later cause haematoma to lyse causing rise in ICP over time
61
What is a subarachnoid haemmorage?
Rupture of arteries from circle of willis berry aneurism, sudden sever onset photophobia thunderlap headache, rapidly fatal and commonest souce of organs for transplant
62
What happens in subarachnoid haemorrage to cause death?
blood causes vasospazm and ischaemia all over the brain
63
What is meningitis?
Inflammation of the meninges,
64
What are the causes of meningitis?
Bacterial viral funcal parasitic, paraneoplastic drug side effects and autoimmune
65
How can CNS be infected?
Direct contiguous spread from sinutes area, or from neurosurgery or trauma and via the blood stream
66
What is the pathophysiology of meningitis?
Blood vessels dilate when pathogen are in CSF, the macrophages and fluids into the CSF and brain and cause inflammationsometimes it isnt in the brain but othertimes it can get into the brain
67
What are symptoms of meningitis?
Fever headache and neck stiffness also nausea vomiting photophobia (irritiabilty confuson delirum and coma indicating severe disease)
68
How serious is meningits?
5% mortality, 20% complications
69
What to do if suspect meningits?
give antibiotics send straight to hospital
70
What are initial steps of management of menigitis?
GCS blood cultures broad spectrum antibiotics, Ceftiaone or ceftaxime steroids to reduce damage
71
What can be tested from lumbar pumcture?
4 samples one to miccrobiology, biochcemistry, microbiology againgram stain cultrue protein Virral PCR microbiology
72
What are the contrindications for Lumbar puncture?
Raised incracranial pressure abnormal clotting profile suspected abcess
73
Why would you do CT in meningitis patient??
When you suspect riased Intracranital pressure
74
When to do CT head before LP?
over 60 immunocompromoised histry of CNS disease, siezures<1 week GCS low focal neurological signs papiloedema, atypical hystory
75
What can cause chronic meningitis?
TB syphilis or cryptococcal fungus or others like parasitic lymes disease parasisc
76
What are causitice organisms of acute meningitis?
Neisseria meningitisi negatice diploccci, sterp pneymonia positieve diplococcia, listeria group strep haemophilisB and ecoli viral herpese smpes varicella zoster enterovirus
77
What guides empirical treatment?
age as different orgamisms are more common. eg neonates usually listeria Group B strep and E coli
78
What is indicative of Bacterial meningitis in CSF fluid?
cloudy high white cell cound pedominance of neutrophils high protein low glucose
79
What is normal CSF like?
clear, acellular WBCC 0-5 cells mm3
80
What is indicative of Viralmeningitis?
high WCCC lymphocytes high high protein normal glucose clear
81
What would be seen in chronic menigitisfrom TB or cryptocccal infectio/
fibrin web lymphocytes high protein low glucose high opening pressure of opening
82
What are DD for meiningitis?
Subarachnoig haemorrage (thunderclap headache), mignaine, flu and other ciral ilnesses, sinusitis, barain abscess and malaria
83
What to do with meningitis that isnt treating the patient?
Contact tracing prophylaxis and nottify PHE
84
What is encephalitis?
Cerebral cortex inflammation
85
What usually causes encephalitis?
Herpes simplex and varicella zoster, tropical travel viruses rabise west nile virus japanese encephalitis paraneoplastc or autoimmune
86
What is clinicalpictues for encepalitis?
consciouness changes GCS low siezures are common focal neuologicalism can sometiems have overlap with meningitis as well
87
How is encephalitis managed?
MRI or CT scan, LP viral PCR, supportive therapy someitiems antiviral,
88
What is tetanus?
caused cy clostridium tetani spore forming from direct innoculation of skin usually in failure to get vaccinated. produce tetanus plasmin that interferes with neurotransmitter relase increased neuron firing causeing muscle spazms
89
What is trismis?
lock jaw
90
What is Risus sardoinicus?
Smile in tetanus
91
What is key in management of tetanus?
supportive antimicrobials muscle relaxants and sedatives tetaus microglobulins to remove toxins
92
What is rabies?
viral infection from animals dogs bats usually spreads via peripheral nerves to CNS long incubation periot 2-weeks 1-3 months is average can get numbness and pain causes very acute syndrome
93
What are the types of rabies presentation?
Furious with spasms and seizures or paralytic weakness and
94
What is treatment for rabies?
There isnt one. 99.9% die. pre-exposure prophylaxias is key and post exposure prophylaxis vaccination and immunoglobulins
Managed with sedatives
95
How does neuromuscular junction work?
Calcium influx in terminal bulb from action potential by voltage gated channels then AcH is released to bind to the motor end plate to cause a muscle action potential
96
How does ACth cause mscle contraction?
IT causes depolarisation of the muscle then the is causes the sarcoplasmic reticulum to release calcium that was stored in it
97
What is myasthenia gravis?
Autoimmune condition agiand AChreceptor and MUsk part of the complex 80-85% are generalised and 50% include occular are positive or ACHR antibodies
98
How much or AChReceptors neeed ot be blocked for symptoms?
60%
99
What are the clinical features of MG?
Extra occular weaknes droopy eyes double visision. limb and bulbar weakness nasal speech dysarthria swallowing difficulties weak chewinf, worsening weakeness after prolongued and sustaind contraction fatiguability is hallmark, tendon reflexes and sensations are normal
100
What can cause complex opthamoplegia?
motorneyronitis multiplex diabetes plyarteritis nodosum amyloidosis, graves disease the muscles botulism kearns-sayre sydrome miller fish syndrome MF
101
What is ice pack test?
get an ice pack pu over the eye leave for a minute if the is improvement that is positive
102
What is Cogan's lid twitch?
move pen up and down wont stop at midline and twitches
103
What are the subgroups of myesthenia gravis?
ocular myasthemia gravis, early onset AChR-myesthenia gravis, late onset AChR mysasthenia gravis, MuSK-myasthenia gravis seronegative myasthenia gravis
104
what is relevance of the thymus gland in myasthenia gravis?
Hyperplasia in early onset generalised myesthenia gravis
105
How is MG diagnosed?
History and examination EMG single fibre EMG repetitive muscle stimulation results in decremental potential highly sensitive single fiber EMG increased jitter and block specific antibody tests
106
Why do Myasthenia gravis need CT chest?
Tocheck thymus
107
Why is thymus important in Myasthenia gravis?
usually atrophys in adult life but can remain large in adult hood, can cause immune cell lymphoid hyperplasia some have thymoma
108
What is a myasthenic crisis?
Leads to respiratory failure impared swallow severe limb weakness one or all of these. 10-15% within 2- years of diagnosis MuSK are more comon quiet breathing reduced chest expansion tachycardia hyertension sugesting hypoxia ABG and sats can be normal. FVC needed or single breath count. Slow vital capacity if less then 1lite
109
What can precipitate myasthenia gravis crisis?
infections stress trauma withdrawal from drugs, rapid introduction of steroids electrolyte imbalace antibiotics antrheumatic drugce antihypertensives botulinum toxin
110
What is the pharmacological management of mysasthenia gravis?
Acetyle esterase inhibitors pyridostgmine. steroids for a bit then asathioprine ciclosporin methotrexate Retuximab if resistant to stop autoantibodies
111
What can help patient in myasthenia gravis crisis?
Plasma exchange immunoglobulin thymectomy
112
What is Eaton lambert syndrome?
Calcium channel antibodies to stop the movement of ions
113
What are brain tumours?
there are 150 types there are neuroepithelial cells can be in neurones or glial cell tumours, there are aastrocytes, oligodendrocytes and there are gliomas like astrocytoma oligodendrocytomas there are meninciomas craniophayngiomas germ cell tumours shwann cellomas lymphatic also secondary ones
114
What is the classification for brain cancer?
Not tnm as done metastisise. based on histology and molecular markes and genetic factors gradine 1 to 4 benign to malignant
115
What are grade 2 tumours of the brain?
slow growwing but will transform at some point in life
116
What affects brain tumour prognosis?
Size tumour kinetics, histology and molecular markers
117
What are the high grade gliomas?
Can be transfromed from 2 but can be new make upmost of brain cancers 85% survival can be from 2-5 years
118
What is the cause of brain cancer?
usually iatrogenic. Radiation therappy 5% family history neurofibromatosis tuberose sclerosis von hippel lindau, Immunosuppressions CNS lymphoma
119
How to brain tumours present?
Deends on what is grade and where generally headache sizures foca neurological symptoms and non focal
120
What is the type of headache in tumour?
Not really raised intractanial raised in morning and worse wih lying down associated n&V coughing and sneesing 24% first symptome 46% have at presentation only 2% only have headache
121
What is highest positive predict for brain tumour?
New onset siezure
122
What should red flag with headache?
headache with old age new or changed or previous history of cancer
123
What are focal brain symptoms?
symptoms that are associated with a specific brain area
124
What are focal symptoms?
Weakness sensory loss ataxia progressive
125
What are non-focal symptoms?
personality change or behaviour memory disturbance or confusion
126
how many people with tumours have siezures?
>80%
127
What are signs of bran tumpur?
Papilloedema, hemiparesis visual field defect dysphasia
128
What are typical signs of low grade?
Siezures often incidental
129
What are the presentation of high grade tumours?
rapidly progresive neurological deficeite symptoms of raised intracriala pressure
130
What are red flags for brain tumour?
headache with focal nwurology, visual field defects, 6th nerve palsy papiloeema nwe onset focal siezure rapidly progressive focal neurology past history of cancer
131
What are Brain tumour investigation?
CT with contrast (but not good at ruling out) MRI much better especially pituatary FMRI for planning surgery
Biopsy/ surgery to work out which one it is
132
What to do when spot a brain tumour?
Histology molecular markers and genetics from a brain biopsy
133
What is treatment for brain tumours?
depends on grade and site and size it is non-curative unless grade 1
134
What are the high grade treatmetns?
Steroids to reduuce oedema, surgery, radiotherapy chemotherapy, temozolamide PCV
135
How are low grade tumours treated?
Surgery early resection radiotherapy and early chemotherapy can get survival from 7.8 to 13.3
136
What is an awake craniotomy?
assessing function during the operation to allow for preservation of function better removal and decreased risk of harming a patient
137
What can be red herrings of non sinister origins?
long histories other functional symtoms
138
What are backgrounds of lambert eaten myasthenic syndrme?
Its rare affecting NMJ and autonomic ganglia, Ab agains PQ type channels and 50-60% have underlying malignancy non cancer is associated with Type 1 DM and thyroid diseases present
139
When do LEMS present?
Non cancer are any age, otherwise over 50
140
What is presentation of Lambert eaton myasthenic sydrome?
Typically proxiamal muscle weekends and dry eyes dry mouth sexual dysfunction autonomic involvement also strength may increase with repeated effort rapid porgressione arly distle muscel involvment and ED
141
What are investigations of LEMS?
90% have antibodies to calcium channel and lots have small cel lung cancer RMG shows reduction on CMAP and subsequent increase of more than 100% with repeated stimulation
142
What is management of lambert eaton myasthenia?
Diamino pyridine helps bloc K and steroids help also treat cancer will help ACh esterase inhibitor
143
What is congenital myasthenic syndrome?
Not autoimmune due to mutation in NMJ proteins
144
What is neuromyotonia?Isacc;s syndrome
Peripheral hyperexcitibility, hyperhydrosis fasiculations crams, myokymia exercise intollerance from antibodies to potassium channels,
145
What is multiple sclerosis?
Inflammatory demyelinating disease specific to CNS usually begins between 20-40 years relapse and remitting but progressive
146
What does relapse and remitting mean?
Random attacks fmroe frequent in first 3 or 4 years recovery can cary disabilities accumulate
147
What are the factors influencine MS?
Genetic environment and chanch clear evidence for environmental factors (twin studies)
148
What is epidemiology of MS?
It varies a lot from country to country but affects wome more than men and white more than black
149
What is the pathophysiology of MS?
genetic succeptibility leading to activated aurto T lymphocytes and B lymphocytes becoming activated and compliment and macrophages causing demyelination
150
What is thecharacteristic damage in MS?
the myelin sheath is damaged and then it is remyelinated with short interndes and thin layer
151
What are the features of active MS lesions?
Demyelination, variable oligodendrocyte loss, hyercellular plaque edge due to infiltation of tisssue with inflammatory cells, perivenous inflammatory infiltrate blood brain barrier distruption central gliosis
152
what are the features of inactive MS lesions?
Demyelination, variable oligodendrocyte loss, hypocellular plaque less inflammation minor blood brain barrier losss
153
Where can MS lesions affect?
Many places but cerebral hemispheres giving silent and variable symptoms, spinal cord leading to tingling numbness snd paraplegia also bladder and sexual dysfunction, optic nerves with vision problems medull a and pons nystagmus vertigo cerebellar white matter dysarthria nystagmus intention tremmor
154
What are typical symptoms of MS?
Optic neuritis impaired vision and eye pain, spacticity and pyramidal sings, sensory symptoms and signes Lhermitte's sign nystagmys double vision and vertigo Bladder and sexual dysfunction
155
What are some atypical presentatins of MS?
Aphasia, hemianopia, extrapyramidal movement disturbance, severe muscle wasting muscle fasiculation
156
What are the usualy first symptoms in MS?
Weakness and parasthesia visual loss and incordination
157
What ar the classifications of MS?
Relapse remitting, primary progressive, secondary progressive or progressive relapsing
158
What is needed to diagnose MS?
Two or more CNS lesions dissminated in time and space exclusion of conditions giving a similar clinical picture
159
How is CSF of MS patients analysed?
Electrophoresis to loog fo IgG banding
160
What are common disease mistaken for MS?
SLE Primary sjogren's syndrome bechets disease polyarteritis nodosa acute disseminated encephalomyelitis, Lye disease syphilis AIDS andrenomeloneurpathy mitochondrial encephalopathy, arnold-Chiari malformation olivopontocerebellar atrophy stroke
161
What are treatmeent for MS?
Cant cure just slow progressions. might be able to modify interferon beta glatiramer dimethyl fumarate and terifunommide are first line methylprednisolone in acute relapse
162
What are other treatmetns for MS?
treating the effects of the lesions themselves such as spacticity
163
What are the lesions to be treated in MS?
Spacticity, tremor (orthotics drugs) sexual dysfunction, depressuon anxiety autonomic dysfunction fatigue
164
What are charateristics of fatigue in MS?
different to normal exacerbated by heat, improves by cold makes other symptoms appear worse
165
What can cause pain in MS?
Trigeminal neuralgia tonic siezures tic like or burning dysaesthetic pain optic neuritis, vertebral compression fracturs ulnar and eroeal palsise chronic joind and back pain painful spazms
166
What are paroxysmal symptoms of MS/
breif duration occur frequently often similar timing to exacerbations, positive sumptoms triggered bu factors can be treated with anticonfulsant
167
What can cause blackouts?
heart relates problems or low blood pressure, (stress-related non-epileptic seizures) hypoglycaemia storke or TIA systonia migrain benign paroxysmal positional vertigo, cataplexy, hyperventialtion, nonepileptic siezure
168
What is an epileptic siezure?
Paroxysmal event which changes in behavour sensation of processes are caused by excessive hypercynchronous neuronal discharges in the brain
169
What are the charicteristic symptoms of an epileptic attack?
30-120 seconds positive additional sensations ictal sumptoms postictal symptoms, can be in sleep , rhythmic jerking often lose control of bowel. tounge bting muscle pain cynaosis can be specific but not sensitive
170
What indicates nonepileptic attack?
situational, longer usually 1-20 mins waxing waning course rapid or very slow posticta recovory may have history of somatofomr disorders, dramatic motor phenomina eyes closed ictal crying or speaking
171
What is syncope?
Paroxysmal even in which changes in bahaviour sensatin and cognitive processes are cause by insuffficeint blood or oxygen supply to the brain
172
What to consider when treating patients with epilepsy?
Is it actually epilepsy, is treatment indicated, what type of epilepsy is it what is the most appropriate drug?
173
What ar the types of epilepsy?
Generalised and focal provoked or unclassified
174
What dictate they type of siezure?
The location of the sizer beginning
175
What is treatment for focal epilepsy?
Carbamazepine or imotragine
176
What is idiopathic generalsied epilepsy?
no associated brain abnormality, manifestation usually under 30.
177
What are types of seizures in idiopathic primary generalise epilepsy?
Absence siezures primary generalised tonic clonic.
178
How do anti epileptic drugs act?
on the synapse on voltage gates sodium channels n presynaptic, noeurotransmitter release, potasssium channels or calcium channels some gaba receptors some gaba transaminase or gaba transporter to increase inhibitions
179
How are anti epileptic drugs intrduced?
Monotherappy to increase to lowest possible effective dose, then increase to fully effective maximum tolerated dose can use combination
180
How effective are anti epileptic drugs?
63% are siezure free but may take a while to find it
181
What are common side effects of anti epileptics?
Significant cognitive side-effects, long term side effects, teratogenic, hepatic enzyme induction non-linear pharacokinetics drug interaction
182
What to do if epilepsy is uncontrolled by drugs?
Vagal nerve implant stimulation (paliative), removal of siezzure prne area very effective if done right
183
What are the types of inflammation on MS?
Macrophage, antibodies distal oligodendropathy apoptotsis and rimary oligdendroglia degeneration
184
What are investigations of MS?
MRI scans Lumbar puncture for CSF immunoglobulins
185
What are phases of MS?
Preclincial radiologically isolated. relapsing remitting and the progressive there isnt much to do inprogressive phase
186
What affects prognosis of MS?
men worse than men late presentation early motor symptoms, shrot inter attack interval high resuidual disabilty
187
How are relapses treated/
type 1 methyl prednisilone type 2 will response to plasma exchenge.
188
When are relapses treated to prebvet?
if have 2 or more in 2 years, interferon Beta prevetion of immunoactivation, modicfying lymphocyte traffcking anti adhesion, Lymphocytes depletions immune reconsitiution with stem cell transplantation
189
What are the characteristics of syncope?
Typically from sittion or standing rarely from sleep presyncopal symptoms, duration 5-30 seconds recovery within 30 seconds cardiogenic has less warning history of heart disease
190
What is the most common brain cancer?
astrocytoma diffuse ones
191
Where are childhood children often?
Posterior fossa
192
What is larges group of CNS tumours?
Neuroepithelial, ependymal oligodroglial astrocytic embryonal pineal choroid plexus also meningeal tumours lymphomas(EBV) germ cell tumours
metastatic tumours
193
What is most of clinical manifestation of brain tumours?
Depends of location of tumour, siezures Raised intracrainial pressure
194
What is diffuse astrocytoma?
infiltrates diffusly and has propensity to undergo progresive anaplasia can't cure cant resect all of it
195
Which grades of brain cancer cannot be cured?
grade 2-4
196
What marks progression of astrocytome?
hypercellularity pleomorphisms, mitoses and necrosis and vascular proliferation
197
What is ISH1?
Isocitrate dehydrogenase mutations
198
What is improtance of IDH1 in brain tumours?
IDH mutation is associated with a better prognosis in gliomas because it is not de novo
199
What is the importance f IDH and oher genetics?
The add to histological view of prognosis for patients
200
What are medulloblastoma?
Primitive small blue cell tumour of the cerebellym childhood, high malignant but can be cured by removal
201
What happens as tumour size increases?
compensation hphase of reduction in ventrical volume and less CSF volume, then after this get somewhat expnential changes in pressure (intracranial pressure) Displacement of tissue happens
202
How does the tracts get affected in brain tumours?
Get displacement of structures by tumours, can cause hydrochepalus if it blocks the ventricle flow
203
Where can herniation happen in the brian?
through the tentorium cerebeli, and the framen magnum
204
What defines headache disorder?
Cephalalgia
205
What are the tyes of headache?
Priamy mignain cluster tension type, secondary, meningitis haemorage
Nerve pain, trigeminal neuraligia
206
What is secondary headach and when to worry about it.
Over 50s history of HIV cancer trauma change in personality congniticve function vomiting with no other cause
207
What is nemonic for secondary headache?
SNOOP 10
Systemic, neurological, onset sdden onset age 50 over, phenotype, pattern change, pregnancy, pregnancy, papillodema, painful eue, pathology, prepcipitants posture post trauma painkillers
208
When is immediate refferal for headache?
Tunderclap, siezure and new headache, suspected meningitis, suspected encephalitis, red eye
209
What are red flags for brain tumours?
cancer history, cluster headache, siezure, significantly altered consciousness behavioural change
210
What is needed in history of headache?
SOCRATES history for each one onset duration how long why asking of help, photophobia phenophobia runny nose blocked nose, triggers what do they do, normal/persisting symptoms
211
What can be examined for headache?
Fever, altered conciousness focal neurology fundoscopy, neck stifness/Kernigs sign BP
212
What are migraines?
With and without aura chronicmigraine medication overuse headache
213
What are most common headaches?
Migran med oversue tension type
214
What is migrain without aura?
5 attacks last 4-72 hours tat fill the others, two of unilateral pulsing moderate severe agravatied by hysical activity, during headache nausea and or vomiting and photophobia or phonophobia?
215
What is aura?
a visual or other disturbance missing part of ision zigzag can be followed after 60mins
216
What are tension type headaches?
Mild to moderate, more than 10 over more thean 1 day or onth that are 30 minutes to 7 days, headache is bilateral,jfsdof odsafh dsofhsdoafhasfisdfhiosdhf
217
What are cluster headache?
5 headaches that are severe or very severe unilateral orbital supraorbital and or temporal pain ipsilateral cranial autonomic features attachs from 1 per day to 8 per day, need to rule out other causes
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What is trigeminal neuralgia?
unilateral facial pain, in distribution of trigeminal nerve not beyond it, recurring in atacks to very short or a couple of mins sever intensity, electric shock like shooting stabbbing sharp perciptated by innoculus stimulit to the face
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How are headaches managed?
Accurate diagnosis and manage expectations, lifestyle modifications and trigger management, pharmacological treatments, psychological and behavioural treatments surgical treatments
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What is abortive treatment?
used to take when the headache is coming on to stop it from developing and can take NSAID asprin or paracetamol and can take anti emetics
221
What is preventative treatment?
topiramate or proranolol as preventive also monoclonal antibodies
222
What to do in resistant headache?
wrong diagnosis not effective for the patient compliance with treatment
223
How investigate sub arachnoid haemorrage?
CT scan and lumbar puncure looking for Xanthechromia angiogram
224
What is management of SAH?
A and E and neurosurgery
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How can idiopathic intracranial hypertension be treated?
CSF shunt, toparamide diuretics, high opening pressure
226
What is giant cell arteritis?
Cause of secondary headache, jaw claudication
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What is chronic daily headache?
description of lots of headache can be many causes but can be chronic migraine or medication overuse headache
228
What areas might have problems in neurology?
Cerebral hemispheres often unilateral, spinal cord(dermatome myotome) cerebellum discoordination, brian stemm cranial nerve palsies crossed modalities, peripheral nerves glove and stocking
229
How is investigation questions in neurology?
where is the lesion what is the pathology
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What's a surgical 3rd nerve palsy?
Pressing on fibres lose parassympathetic
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What a medical 3rd nerve palsy
might not lose parasympathetic
232
What is internuclear opthalmoplegia?
Looking to one side asymetrical nystagmus as it moves to object lesion of medial longditudinal fasiculus from loss of
233
What is lateral medullary syndrome?
infarct to brainstem Ipsilateral horners limb at
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What is weakness?
impared ability to move a body part in the will to move it
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What is paralyiss?
Inability to move a body part in response to will
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What is ataxia or incoordination?
Willed movements are clumsy ill-directined or uncontrolled
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What are involuntary movementes, spontaneous movement of a body pary independently of will
What is apraxia diorder of consiously organised patterns of movement or impared ability to recall acquird motor skills
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Where are lower motor neurons?
Located in the anterior horns of the spinal cord and cranile nerve nuclei in the brainstem
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What innervates stretch receptors?
Gamma motor neurones
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What happens in LMN lesions?
Reduced tone flaccid muscle wasting reduced reflexes and fasciculations
241
What diseases affect LMN?
MND SMA poliomyelitis syringomeyelis syringobulbia spinal cord brainstem compression vascular disease
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What can affect peripheral nerves?
Distal weaknes glove and mononeuroitis mutiplex axonel degeneration
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Where do myopathies present?
Closer muscles
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What is pyramidal tract weakness?
general weakness, Decreased control of active movement slowness, spacticity velocity dependant cnage in muscle toneimb preservation of flexion in lower limbs
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What happens in upper motor neuron lesions?
increased tone or spacticity, tendon reflexes are brisk, planter responses like babinski sign get muscle weakness but with upper limbs extensorts weaker than flexors but lower limbs flexors weaker than extensors, finer more skillful movements severely impared and may ger emotional lability bay be present
246
What can be affected in upper motor neurons?
Cortical lesions Internal capsule Brainstem Spinal cord
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What can be affected in upper motor neurons?
Cortical lesions Internal capsule Brainstem Spinal cord
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What does muscle wasting show?
Lower motor lesion, not MS
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What affects muscle tone?
The feedback from stretch receptors and golgi tenton organs.
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What are the sites of lower motor neuron damage?
motor nuclei of cranial nerves, motor neurones in the spinal cord, spinal ventral roots, peripheral nerves Neuromuscular junction
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What are signs and symptoms of MND?
Muscle atrophy in limbs fasiculations, split hand FDI wasting tongue wasting respiratory
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What can cause damage to motor neurons of the spina; roots?
Prolapses intervertebral disc, cervical or lumbar spondylosis, tumours(neurofiibroma and ependymoma) Malignant infiltration,
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What can cause problems with peripheral nerves ?
symmetrical polyneuropathy from diabetes or B12
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How can you locate the site of the lesion in motor neurons?
Knowletege of reflexes anatomy o f innervation of muscles, sensory and motor signs?, history of diurnal variability/fatigueability, fasciculations patterna of weakenss
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How should LMN be investigated?
Neuro-imaging MRI scan head spine neurophysiology, Blood testes muscle enzymes peripheral neuopathy screeen auto-antibodies lumbar puncture
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Where in the brain might there be upper motor neuron lesions?
Cortical lesions, internal capsule, brainstem and spinal cord
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What do cortical lesions lead to?
contralateral circumscribed weakness,
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internal capsule injury leads to/?
complete contralateral hemiparesis, descending fibres grouped closesly together in a very small area
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What happens in brainstem lesions?
Often bilateral weakness due to involvement of both descending corticospinal tracts may have cranial nerve involvment or bulbar envolvement
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Spinal cord lesions lead to ?
bilateral corticospinal tract lesions cervical will involve upper and ower limbs below cervical will be legs sensory level may help localising the site of the lesion
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Which diseases affect upper and lower motor nerones?
MND hereditary spastic paraplegia
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What are investigations for upper motor neurone problems?
MRI, blood tests for metabolic disorders CSF examination
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What is TLOC?
Transient losss of concessioness Spontaneous loss of consciousness with complete recovery
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Why is it important to investigate TLOC?
To find if its cardiac or neurological as they have higher mortality
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What are the challenges of TLOC investigation?
Main witness unconsiious so hard to know what happened, unpredictable occasionally life threatening, driving restrictions health and safety
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What are caues of TLOC?
Syncope (vasovagal, situational, orthostatic hypotension, cardiac), seizure and Non-epileptic attack disorder
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What are the key questions of TLOC?
What do they mean by black out. was there a trigger prodrome the attack and recovery how often does it happen
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What can help about prodrome?
atypical aura, pre syncopal loss of vision, provoking features assocciated symptoms what are the circumstances can they be prevented
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What is important to know about the attack?
did they lose consciousneess, how long was it change in complexiona verbal responsiveness, feel pulse, movemet jerking injuries
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What is important about the recovery?
Rapid or prologued confused or sleepy muscle pain, how much does they remember
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What is vasovagal syncope?
from standing up due to drop in BP PPP upright provocation, becom pale sweaty vision blurred hearing mufled brief duration reduced muscle tone and rapid recovery. can be convulsive but not typical,
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What is a key differentiation for vasovagal?
No post ictal confuusion often happens when standing up from sitting or lying
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What is cardiac syncope?
Sudden temporary reduction of blood supply to the brain and hence oxygen to the brain, this can be from vasodilation hypotension and arrhythmia
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What is it important to do if you suspect cardiac syncope?
ECG ask about arrhythmogenic drugs family history of cardiac disease or sudden death
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What is typical of epilepsy?
An aura dejavu olfactory or gustatory maybe visual, lsts 30 seconds to 180 seconds, prolongued post ictal confusion, head turning or posturing of body, stiffening of body and myoclonic jerking, abnormal behaviour of which patients do not remember, severe tongue biting
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How are siezures described?
They are described as the seizure types, epilepsy types epilepsy syndromes and aetiology
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What is a focal siexure?
Originate within networks limited to one hemisphere, may be discretely localized or more widely distributed
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What is a generalised siezure?
Originate in a pointbut rapidly engages networks bilaterally, can incluse cortical and subcortical structures doesnt have t be entire cotex
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Is a TIA TLOC?
No as doesn't actually usually cause a loss of consciousness
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What is TEA?
transient epileptic amnesia doesnt involve loss of consciousness
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What is likely to indicate Non epileptic attack disorde?
gradual onset undulating motor activity with pauses, sinusoidal and asynchronous arm and leg movements prolongues atonis rhythmic pelvic movemnents sitde to side headd mviements, ppost ictal crying prlongued with fast recovery waxing waning course
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What is helpful vs not helpful in history?
Scant description frequent or long siezures different types of siezures crying during recovery is helpful, injury tongue biting and incontincence and siezures in sleep are not very helpful
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How do you make a diagnosis of non epileptic attack disorder disease?
Description/ nature of siezure changes with time good documantaion, unsually frequent drug unresponsie provoked by stress, histoy of somatoform disorder unexplaind systomes history of personality disorder self harm alcohol abuse self harm childhood abuse ask for a video of it
284
Why is it important to diagnose Non-epileptic attack disorder?
Inappropriate to start AED as will have no effect, there is treatment for non epileptic attack disorder, reinforcement of abnormal illness behaviour evolution of functional symptoms, incapacity financial and social dependency
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What to do with TLOC in A and E or GP?
TLOC clinic with cardiology, ECG, first seizure clinic, advice on driving safety
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When is EEG indicated?
not to investigate blackout, when wanting to determine epilepsy type or for non epileptic attacks, helpful to capture recording
287
When is an MRI indicated in epilepsy?
To look for structural abnormalities
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How can head injuries be classified?
Type of injury penetrating or blunt injuries, distribution of the lesions focal or diffuse or time course of damage follwing the traumatic event primay from injur or secondary after the event
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what is a scalp laceration?
A tear to an area of skin not from a sharp object indicates something severe has gone on
290
What is involved in skull fractures?
Imples considerable force increased risk of haemotoma, infection or aerocele flat surface njuries cause flat linear fractures and sharp form distinct flocalised depressed fractures
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What is an extradural haematoma?
From a skul fracture and develops over a few hours often from middle meningeal artery, 10% of head injuries causes death by raised ICP
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What cause subdural haemotomae?
bridging veins rupturing can be chronic
293
What can cause rapid cognitive deline?
dementia but also subdural haematoma which can be treated
294
What can cause subarachnoid haematoma in injuries?
contusions and lacerations of the meningeal layers or skull fracture, dissection or rupture of the vertebral artery
295
How does head injury get infection?
Skull fracture provides a way to let bugs in
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What are the focal brain damage mechanism?
Contact damage or accelleration or deceleration damage
297
What is contact damage?
At or just deep to the point of impact
298
What is a coup contusion?
Brain damach at the site of lesions happens on the crests of the Giri
299
What is a contrecoup contusion?
One on the opposite side to the site of the blow to the brain of the coup mainly jsut from the skull being very close to the underside of the brain
300
What are diffuse lesions?
Diffuse axonal vascular swelling vvascualer
301
What is traumatic axonal injury?
can be focal or widespread can be from ischaemia and damage from acceleration often in rotational injury in brainstem
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What does traumatic axonal injury look like?
Spheroids of swollen axons, causing build up of amyloid at the site of damage
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What does traumatic axonal injury look like?
Spheroids of swollen axons, causing build up of amyloid at the site of damage can be mild or severe
304
What are the effects of traumatic axonal injury?
discolouration of brain and loss of white matter tracts, can also damage blood vessels and cause bleeds petechial bleeds
305
What is brainswelling/
Occurs very often in the brain after injusry raises intracrannial pressure from congestive brain swelling vasodilation and cerebral blood volume, vasogenic oedema or cytotoxic oedema release of proteins in CNS casing swelling
306
What can be squished in the tentorial incisure?
The uncus in the media temporal lobe
307
What happens in the foramen magnum in raised ICP?
herniation of tonsl of cerebellum and pressure on the medulla
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When do you get hypoxic ischaemia of the brain?
Hypotension for a while raised intracranial pressure can be widespread or confined to vulnerable regions border zones between major cerebral territories
309
what visible things can you see in the brain with ischaemic hypoxia?
de distinction of the white and grey matter
310
What can happen after years of injury?
More likely to develop epilepsy
311
What is chronic traumatic encephalopathy?
from trauma, boxers and rugby players. 12% of adults have had a traumatic brain injury with loss of conciousness it is a risk factor for dementia and chronic traumatic encephalopathy
312
Chronic traumatic encephalopathy presentation?
Irritibility agression and memory loss then dementia and parkinson like symptoms and MND but have Tau deposition and TDP-43 but in strange patterns not like
313
What are the two main types of stroke?
Haemorrhagic stroke and ischaemic stroke
314
What are the two areas you can group cerebral events/
is it a posterior or anterior circulation stroke?
315
What is the most damaging area to have a stroke in?
Middle cerebral is really bad as does a lot cause high deficiet
316
What are the characteristics of anterior circulation teritory stroke?
leg weakness, sensory disturbance in the legs, Gait apraxia truncal ataxia, incontincence drowsiness, Akinetic mutism decrease in spontaneous speech stupurus state
317
What does a stroke look like on a scan?
darker area as it is less dense from exocutotoxicity and the cells swell/retain water
318
How long does it take for stroke to show on a CT scan?
4 or so hours
319
What do you get with a middle cerebral artery stroke?
Contralateral arm and leg weakness, contralateral sensory loss, hemianopia, aphasia dysphasia, facial droop
320
What happens in large middle cerebral artery strokes?
Displacement of ventricals, mallicangnant MCA syndrome causing coning
321
What are symptoms of posterior cerebral artery stroke?
Contralateral homonymous hemianopia, Cortical blindness with bilateral involvement of the occipital lobe branches, visual agnosis prosopagnosia dyslexia anomic aphasia colour naming discrimination problems headaches unilateral
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Which are worse anterior circulation or posterior circuation?
Posterior as stops signals getting down
323
What is common signs of posterior circulation strokes?
Motor deficits such as hemiparesis or tetraparesis and facial paresis, dysarthria and speech swallowing impairment vertigo nausea vomiting, visual disturbances, altered consciousness
324
What kind of scan for posterior?
MRI as shows the water content of the brain so can show areas more clearly
325
What is lacunar stookes?
They affect one modality often
326
What are warning syndromes?
Symptoms that are warning of stokes happening fluctuating symptoms from reperfusion
327
What are the treatments for stoke?
break up the thrombotic embolus, or thrombectomy to remove the thrombus
328
What are conditions for thrombolysis?
IV treatment, up to 4.5 hours after onset, cant have if had recent surgery, recent arterial puncture, hisory of active malignancey evidence of brain aneurisms, patient on anticoagulation severe liver disease acute pancreatitis liver disease or has a clotting disorder
329
What are the two types on neurological motor disorders?
Physical problems Parkinson's Huntington's, Also software problems, essential tremmor, dystonia and tourette's
330
What are the usual presentations of Parkinson disease
Initial gate problems and gradual worsening of symptoms on one side of the body, wehen walking drag leg walk slowly, stiffness reduce armswing, importance of time progressive but not always there, affects one side more than the other later might have both
331
What are the three cardinal features of Parkinson's?
Brady/Akinesia(typing buttons smaller writing walking deteriorated, tremor at rest may be unilateral, rigidity pain problems with turning in bed
332
What are important examination findings of Parkinson's?
small stepped gait with stooped posture reduced armswing one side more than the other, increased tone=regidity, tone increased over entire radius of joint movement, rest tremor with frequecy 3-6HZ, often asymmetrical also some postural tremor, decreasing amplitude/accuracy of repetitive movements much better at the beginning gradual worsening
333
What causes pathology in parkinsons?
intracytoplasmic inclusion bodies Lewy bodies in the substantia ngra cells
334
What is DaTSCAN?
Radiolabelled ligand for the substantia nigra end of neurones and find signal is reduced in Parkinson's not necessarily specific
335
What are causes of Parkinson's?
Risk factors, Toxin induced, Parkinson's genes, susceptibility factors, mitochondrial dysfonction, oxidative stress causing cell loss in the substantia nigra
336
What to do to speak to patients about prognosis of parkinsons?
It is slowly progressive, it does not change its nature over night you are the expert
No cure no disease modifying treatment but plenty of symptomatic treatment options compensate for loss of dopamine
337
What drugs for Parkinson's?
L-dopa a precursor to dopamine, Dopamine agonist to act on the recptors also monoamino-oxidase inhibitors and catechol-o-methyl-transferase to stop break down
338
What are the use of anticholinergics for Parkinsons?
Block the parasympathetic to allow mroe effect of dopamine, they affect cognition, and others
339
What are the motor complications of late-stage PD?
Wearing off medication doesnt work for as long, on-dyskinesia hyperkinetic choreiform movements when work, off dysckinesia painful dyskinesia and losss of function
340
When should you treat parkinson's?
depend on symptoms, not sure it makes an effect on disease
341
How to chose which drug?
inhibitors are not very powerful, agonist first line in younder good for soft sideeffects like tirednes gambiln hypersexuality and L dopa is most powerful and go to, greater risk of SE
342
What are types of L-Dopa?
dispersible kick start in morning standard release for day time slow release for night time
343
What is cognitive disease in PD?
Depression very common, other psyciatric problems phobias, aniety hallucialtion autonomic problems constipation increased urinary frequency urinary incontinence not typical denentia
344
Which signs are not usually present in Parkinson's?
Dementia, symmetry, early falls, incontinence
345
What is in the sensory ganglion?
the cell bodies of the sensory neurones which lie out of the spinal cord
346
What fibres carry pain?
C fibres and A delta fibres
347
What fibres cary light touch and pressre?
ABeta
348
Which nerves carry propriaceptopn?
Aalpha
349
What can cause nerve damage?
Demyelination or axonal damage
350
What is mononeuopathy?
Problem with one nerve
351
What is polyneuopathy?
Problem with multiple nerves
352
What are common mononeuropatheis?
Carpal tunnel syndrome ulnar neuropathy cubital tunnel, peroneal neuopathy entrapment at fibular hedcranial nerve palsys
353
What are the two main types of polyneuropothies?
Large fibre neuropathies or small fibres
354
What are the types of large fibre neuropathties?
Chronic or acute axonal or demyelinating
355
Which fibres are most likely to be affected first?
temperature and pain from small C fibre loss
356
What is ataxia?
Poor balance sensory loss of proprioception or cerebellar dysfunction when sensory it gets worse with eyes closed
357
What are motor symptoms of peripheral europathy?
Muscle cramps, high arch foot weaknes fasiculations and atrophy
358
What cause asymmetrical sensory?
patch distribution, dorsal root ganglia affected uncommone part of paraneoplastic, Sjogren's Gluten sensiticity
359
What causes asympetrical sensorimotor?
vasculitis, mononeuritis multiplex
360
What causes symerical nerve los?
length-dependent initially sensory but sensorymotor often from diabetes B12
361
How to make a diagnosis of peripheral neuropathy/
History, clinical exam sensory and motor deficites, reduced or absent tendon reflexes neurophysiolocgical examinations
362
What differentiates demyelinating from axonal loss?
slow conduction axonal is reduced amplitudes of the potentials in NCS
363
What can cause axonal PN?
systemic disease (b12 diabetes CD CKD alcohol hypothyroidism amyloidosis connective tissue disease HIV hepatitis immune mediated vasculitis diabetes metabolic disorders pharmaceuticals hereditary
364
What are the chronic demyelinatice neuropathies
Charcot marie tooth disease umbrella term all genetic, Hereditary
365
What are the acute polyneuropathies?
Guillain Barre syndreme
366
What is guillian Barre syndrome?
Demyelinating Axonal motor axonal sensorymotors rapid ascending paralysis and sensory deficits, infection might proceed it needs immediate treatment ICIG plasma exchane ITU
367
What can cause death in guillian Barre syndroem?
autonomic failure infection or non-creatment
368
How are neuropathies treated/
pain amytriptiline cramps with quinine balance through physio usually symptomatic also aim to identify the cause and treat
369
What is involved in risk management of stoke post stroke/
Aspirin and clopidogrel, statins AF treatment warfarin NOAC'srivaroxabam Blood pressure treatment
370
What are other stroke treatments?
Clot retrieval thrombectomy, intraarterial thrombolysis decompressive craniectomy
371
What to do with stroke straight away?
CT head
