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Year 3 - Neurology (DP) > Parkinsons and MS > Flashcards

Parkinsons and MS Flashcards

1
Q

What bacteria can cause a chronic bacterial infection in the CNS?

A

TB

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2
Q

What is acute encephalitis?

A

Infection of the brain parenchyma

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3
Q

In a grossly pyogenic meningitis, what does the thick layer of suppurative exudate cover?

A

The leptomeninges (pia and arachnoid)

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4
Q

What can be seen microscopically in grossly pyogenic meningitis?

A

Neutrophils in subarachnoid space

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5
Q

When is viral meningitis most common?

A

Late summer/autumn

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6
Q

What is the most common cause of viral (aseptic) meningitis?

A

Enteroviruses (eg. ECHO virus)

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7
Q

What investigations can be carried out in viral meningitis?

A

Viral stool culture
Throat swab
CSF PCR

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8
Q

What is the most common cause of viral encephalitis?

A

Herpes simplex virus

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9
Q

What is another important cause of viral encephalitis? What important feature of their past medical history could suggest this?

A

Varicella zoster

History of shingles

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10
Q

How do we treat the two main causes of viral encephalitis?

A

High dose aciclovir

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11
Q

When must the commonest cause of viral encephalitis be treated?

A

<6 hours after admission

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12
Q

What three travel related viruses can cause encephalitis?

A

West Nile
Japanese B encephalitis
Tick borne encephalitis

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13
Q

What are the clinical features of viral encephalitis?

A 
Insidious (sometimes sudden)
Meningismus (meningism)
Stupor/Coma
Seizures and partial paralysis
Confusion/Psychosis
Speech and memory symptoms
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14
Q

How can we investigate viral encephalitis?

A

LP
EEG
MRI

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15
Q

What are the MRI findings in viral encephalitis?

A

Inflammed temporal lobe is brightest white:

  • Uncus
  • Adjacent parahippocampal gyrus
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16
Q

What are the commonest causes of bacterial meningitis in neonates?

A

Listeria
Group B strep
E. coli

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17
Q

What is the commonest cause of bacterial meningitis in children?

A

H. influenzae

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18
Q

What is the commonest cause of bacterial meningitis in those aged 10-21?

A

Meningococcal

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19
Q

What are the commonest causes of bacterial meningitis in those aged >21?

A

Pneumococcal > Meningococcal

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20
Q

What are the commonest causes of bacterial meningitis in the elderly?

A

Pneumococcal > Listeria

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21
Q

Those with a reduced cell-mediated immunity (eg. HIV) are more prone to what cause of bacterial meningitis?

A

Listeria

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22
Q

Those who have undergone neurosurgery or have experienced open head trauma are at risk of what causes of bacterial meningitis?

A

Staph/

Gram negative bacilli

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23
Q

In a patient with a cribiform plate fracture, what is the commonest cause of bacterial meningitis?

A

Pneumococcal

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24
Q

Which of the following is not a common cause of bacterial meningitis in immunocompromised patients:

  • Strep pneumonia
  • Neisseria meningitidis
  • Listeria
  • H. influenzae
  • Aerobic gram negative bacilli (inc. Psuedomonas)
A

H. influenzae

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25
Q

Which of the following is not a common cause of bacterial meningitis in patients with a skull base fracture:

  • Staph. aureus
  • Strep. pneumoniae
  • H. influenzae
  • Beta haemolytic GAS
A

Staph. aureus

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26
Q

Which of the following is not a common cause of bacterial meningitis in patients post-neurosurgery/open head trauma:

  • Staph aureus
  • Staph epidermidis
  • Aerobic gram negative bacilli
  • Strep. pneumoniae
A

Strep pneumoniae

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27
Q

Which of the following is not a common cause of bacterial meningitis in patients with a CSF shunt:

  • Staph epidermidis
  • Staph aureus
  • Aerobic gram negative bacilli
  • Neisseria meningitidis
  • Proprionibacterium acnes
A

Neisseria meningitidis

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28
Q

What is a common cause of bacterial meningitis in AIDS patients?

A

Cryptococcus neoformans (when CD4 <100)

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29
Q

In patients with meningitis due to Neisseria meningitidis, where might bacteria be seen in the CSF?

A

Inside leucocytes

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30
Q

How do Neisseria meningitidis gain access to the meninges?

A

Via the bloodstream

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31
Q

What cause the symptoms in Neisseria meningitidis meningitis?

A

Endotoxin

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32
Q

Why are military recruits vaccinated against Neisseria meningitidis?

A

Prevents epidemics in training camps

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33
Q

What are some local disease features (apart from the meningitis) of Neisseria meningitidis?

A

Conjunctivitis

Arthritis

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34
Q

What is the mortality rate of localised Neisseria meningitidis meningitis?

A

5%

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35
Q

What is the mortality rate of Neisseria meningitidis meningitis with septicaemia?

A

15%

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36
Q

What is the mortality rate of Neisseria meningitidis meningitis with fulminant septicaemia?

A

15-40%

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37
Q

What subtype of H. influenzae is the commonest cause of meningitis in children younger than 4 years?

A

Hib

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38
Q

What are the risk factors for pneumococcal meningitis?

A 
Hospitalised patients
CSF skull fracture
Diabetes
Alcoholics
Young children
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39
Q

What is the gram stain and shape of Listeria?

A

Gram positive bacilli

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40
Q

What are the risk factors for Listeria Monocytogenes meningitis?

A

Neonates
Age >55 years
Immunosuppressed (esp. if due to malignancy)

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41
Q

What is the treatment for Listeria meningitis?

A

IV ampicillin/amoxicillin

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42
Q

How can we diagnose cryptococcal meningitis?

A

Serum and CSF cryptococcal antigen

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43
Q

How is cryptococcal meningitis treated?

A

IV amphotericin B/Flucytosine

Fluconazole

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44
Q

Is CSF pleocytosis indicative of bacterial meningitis?

A

No

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45
Q

In what order to we collect CSF tubes?

A

Tube 1 - Haematology
Tube 2 - Microbiology
Tube 3 - Biochemistry
Tube 4 - Haematology

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46
Q

What cells are predominant in CSF in viral meningitis?

A

Lymphocytes

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47
Q

What cells are predominant in CSF in bacterial meningitis?

A

Polymorphs

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48
Q

What cells are predominant in CSF in TB meningitis?

A

Mostly lymphocytes

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49
Q

What is the protein level in viral meningitis?

A

Normal or slightly high

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50
Q

What is the protein level in bacterial meningitis?

A

High

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51
Q

What is the protein level in TB meningitis?

A

High or very high

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52
Q

What is the glucose level in viral meningitis?

A

Usually normal

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53
Q

What is the glucose level in bacterial meningitis?

A

Less than 70% of blood glucose

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54
Q

What is the glucose level in TB meningitis?

A

Less than 60% of blood glucose

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55
Q

What values for the following parameters are highly predicative (99% accuracy) of bacterial meningitis:

  • WBC count
  • Neutrophils
  • Protein
  • Glucose
  • Glutamate (CSF/Serum)
A 
WBC count >2000
Neutrophils >1180
Protein >220mg/dL (>0.22g/L)
Glucose <34mg/dL (<2.125mmol/L)
Glutamate <0.23
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56
Q

What are some non-infectious causes of neutrophilic pleocytosis and low CSF glucose?

A

Chemical meningitis (eg contrast)
Behcet syndrome
Drugs (NSAIDs, Sulfa, INH, IV Ig)

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57
Q

What is the other name for aseptic meningitis?

A

Encephalitis syndrome

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58
Q

What are some indications for hospital admission in meningitis?

A 
Meningism
Impaired consciousness
Petechial rash
Febrile/Unwell and recent fit
Headahce
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59
Q

Which is done first on admission with suspected meningitis, LP or antibiotic therapy?

A

Antibiotics

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60
Q

What investigations are done immediately after empirical antibiotic therapy?

A

Throat swab

Swab/aspirate any rash (microscopy and culture)

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61
Q

When would we undergo a CT prior to LP in meningitis?

A 
Immunocompromised
CNS disease
New onset seizure
Papolloedema
Altered consciousness
Focal CNS deficit
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62
Q

What is the empirical antibiotic treatment for bacterial meningitis?

A

IV Ceftriaxone 2g bd

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63
Q

What antibiotic is added to the empirical treatment of bacterial meningitis if Listeria is suspected?

A

IV amoxicillin 2g qds

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64
Q

What is the empirical antibiotic treatment of bacterial meningitis if the patient has a penicillin allergy?

A

IV Chloramphenicol 25mg/kg 6-hourly qds WITH

IV Vancomycin 500mg 6-hourly (or 1g 12-hourly)

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65
Q

What antibiotic is added to the empirical treatment of bacterial meningitis if Listeria is suspected and the patient has a penicillin allergy

A

IV Co-trimoxazole 120mg/kg into 4 divided doses/day

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66
Q

When are steroids given in bacterial meningitis?

A

To all patients with suspected meningitis

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67
Q

What steroid is given in bacterial meningitis?

A

IV Dexamethasone 10mg:

  • With/Just before 1st antibiotic dose
  • Then qds for 4 days
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68
Q

In what kind of meningitis do steroids have the most benefit?

A 
Pneumococcal
Reduced chance of:
- Impaired consciousness
- Seizures
- Cardio-pulmonary failure
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69
Q

When would steroids not be given in meningitis?

A

Post-surgical meningitis
Immunosuppressed
Meningococcal or septic shock
Allergy

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70
Q

How can we assess prognosis in meningococcal disease?

A 
Haemorrhagic distheses
Reduced consciousness
Multiorgan failure
Rapidly developing rash
Age >60
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71
Q

How can we assess prognosis in all types of meningitis?

A 
Tachycardia
GCS <12
Low GCS, CN palsy
Seizures within 24 hours
Hypotension
Age >60
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72
Q

What are the contact prophylaxis regimens for meningitis for people older than 12 years?

A 
PO Rifampicin 600mg 12-hourly for 4 doses
OR
PO Ciprofloxacin 500mg single dose
OR
IM Ceftriaxone 250mg single dose
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73
Q

What are the contact prophylaxis regimens for meningitis for people older than kids aged 3-11months?

A

PO Rifampicin 10mg/kg 12-hourly for 4 doses
OR
IV Ceftriaxone 125mg single dose

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74
Q

What are pyramidal/UMN features?

A

Pyramidal weakness:
- Weakness of extensors in upper limbs
- Weakness of flexors in lower limbs
Spasticity

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75
Q

What are hyperkinetic motor disease features?

A 
Dystonia (sustained/repetitive muscle contractions resulting in twisting motions and abnormal posture)
Tics
Myoclonus
Chorea
Tremor
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76
Q

What is chorea?

A

Brief, irregular movements that move from one muscle to another

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77
Q

What are hypokinetic motor disease features?

A

Parkinsonism

Parkinson’s disease

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78
Q

What part of the brain do hyperkinetic and hypokinetic motor disease features arise from?

A

Basal ganglia

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79
Q

Where does ataxia arise?

A

Cerebellum

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80
Q

What is ataxia?

A

Loss of voluntary control of muscle coordination (including gait abnormality)

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81
Q

What are the features of Parkinson’s?

A

Rigidity
Akinesia/Bradykinease
Resting tremor
Gait abnormalities

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82
Q

What is ballismus?

A

Chorea motions with large amplitude

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83
Q

What is tremor-dominant Parkinson’s Disease?

A

Relative absence of other motor symptoms

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84
Q

What is non-tremor-dominant Parkinson’s Disease?

A

Akinetic-rigid syndrome

Postural instability gait disorder

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85
Q

Which type of Parkinson’s Disease is associated with slower progression and less functional disability?

A

Tremor-dominant

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86
Q

What are some non-motor features of Parkinson’s Disease?

A 
Olfactory dysfunction
Cognitive impairment
Psychiatric symptoms
Sleep disorders
ANS dysfunction
Pain Fatigue
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87
Q

When are non-motor features of Parkinson’s Disease common?

A

Early disease

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88
Q

What are the advanced stages of Parkinson’s Disease associated with?

A

Emergence of complications due to long-term fluctuations

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89
Q

What are the symptoms of late-stage Parkinson’s?

A

Axial motor symptoms:

  • Postural instability
  • Freezing of gait
  • Falls
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90
Q

During what part of sleep do parasomnias occur in Parkinson’s?

A

REM sleep

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91
Q

How can parasomnias be diagnosed in Parkinson’s?

A

Overnight polysomnography

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92
Q

How are parasomnias in Parkinson’s treated?

A

Clonazepam
Melatonin
(Both at bedtime)

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93
Q

What are the pathological hallmarks of Parkinson’s?

A

Loss of dopaminergic neurones in substantia nigra

Lowy body pathology

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94
Q

What are intracellular inclusions of alpha-synuclein?

A

Lewy bodies

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95
Q

What are the processes of neurones with intracellular inclusions of alpha-synuclein?

A

Lewy neurites

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96
Q

Where are insoluble misfolded alpha-synuclein deposits found?

A

Brain
Spinal cord
PNS

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97
Q

What is the sterotyped progression of Lewy body pathology?

A

6 stages:

  • Starts in PSN
  • Progressively affects CNS in a caudal to rostral direction in the brain
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98
Q

Where does the loss of dark black pigment occur in the brain in Parkinson’s?

A

Substantia nigra

Locus coeruleus

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99
Q

Where is the prevalence of Parkinson’s higher?

A

Europe

North and South America

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100
Q

What is the greatest risk factor for Parkinson’s?

A

Agr

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101
Q

What is the M:F ratio of Parkinson’s?

A

3:2

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102
Q

Onset before what age suggests a genetic cause of Parkinson’s?

A

40 years

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103
Q

What is the greatest genetic risk factor for Parkinson’s? What does in encode?

A

Mutations in GBA
Encodes Beta-Glucocerebrosidase:
- Lysosomal enzyme deficient in Gaucher’s Disease

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104
Q

What mutation is the most common cause of dominant Parkinson’s?

A

LRRK2

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105
Q

What mutation is the most common cause of recessive Parkinson’s?

A

Parkin

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106
Q

What was the first gene associated with Parkinson’s and what does it go?

A

SNCA

Encodes the protein alpha-synuclein

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107
Q

What environmental factors are protective against Parkinson’s?

A 
Smoking
Coffee
NSAIDs
Calcium channel blockers
Alcohol
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108
Q

What environmental factors are associated with an increased risk of Parkinson’s?

A 
Pesticides
Prior head injury
Rural living
Beta blockers
Agricultural occupation
Well-water drinking
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109
Q

What is the main drug in symptomatic treatment of Parkinson’s?

A

Levodopa

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110
Q

Give examples of dopamine agonists?

A

Ropinirole
Pramipexole
Cabergoline

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111
Q

Give an example of a MAO-B inhibitor?

A

Selegiline

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112
Q

When is Amantadine used in Parkinson’s?

A

Relieves dyskinesias

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113
Q

When should treatment be initiated in Parkinson’s?

A

When symptoms cause disability or discomfort

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114
Q

What drugs are better for the more severe symptoms of Parkinson’s?

A

Levodopa

Dopamine agonists

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115
Q

What are more effective therapies for tremor?

A

Anticholinergics
Trihexyphenidyl
Clozapine

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116
Q

What are the side effects of both Levodopa and Dopamine agonists?

A

Nausea
Daytime somnolence
Oedema (Greater in dopamine agonists)

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117
Q

What are additional side effects of dopamine agonists?

A 
Pathological gambling
Hypersexuality
Binge eating
Compulsive spending
Hallucinations
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118
Q

When should dopamine agonists be avoided?

A 
Patients with a history of:
- Addiction
- OCD
- Impulsive personality
Elderly
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119
Q

What is long-term levodopa therapy associated with?

A

Motor complications:

  • Dyskinesias
  • Fluctuations
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120
Q

How can levodopa-related side effects be reduced?

A

By adding:

  • Dopamine agonist
  • MAO B inhibitor
  • Catechol-O-methyltransferase inhibitor
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121
Q

How is psychosis in Parkinson’s managed?

A

Clozapine

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122
Q

How are visual hallucinations and delusions in Parkinson’s patients with dementia treated?

A

Cholinesterase inhibitiors (eg. Rivastigmine)

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123
Q

How can psychotic symptoms in Parkinson’s be managed without affecting motor function?

A

Primavansenin

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124
Q

Apart from moving, how else does bradykinesia affect a Parkinson’s patient?

A

Hypomimia
Hypophonia
Micrographia

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125
Q

What is the frequency of the tremor in Parkinson’s?

A

3-6Hz

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126
Q

How can the resting tremor be accentuated in Parkinson’s?

A

Best observed when patient is focused on a mental task (eg count back from 100)

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127
Q

How can rigidity in Parkinson’s be distinguished from spasticiy in UMN lesion?

A

The resistance to passive movement does not increase with faster passive movement

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128
Q

Where is the “cog-wheel” rigidity most apparent?

A

At the wrist

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129
Q

How can we accentuate rigidity in Parkinson’s?

A

Froment’s manoeuvre:

- Ask patient to voluntarily move another body part

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130
Q

What is camptocormia?

A

Anterior truncal flexion in Parkinson’s

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131
Q

What symptoms should be absent to diagnose pure Parkinson’s disease?

A

Sensory
Pyramidal
Cerebellar

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132
Q

If a patient with suspected Parkinson’s disease has changes in eye movement latency/speed/accuracy, what is a more likely diagnosis?

A

Progressive Supranuclear Palsy with Parkinsonism

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133
Q

What treatable causes of asthenia should be ruled out?

A

Hypothyroidism

Anaemia

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134
Q

What part of the body does vascular Parkinson’s affect predominantly?

A

Lower limbs

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135
Q

What cardinal feature of Parkinson’s is uncommon is vascular Parkinson’s?

A

Resting tremor

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136
Q

What other signs of brain vascular lesion may be present in vascular Parkinson’s?

A

Spasticity
Hemiparesis
Pseudobulbar palsy

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137
Q

Symmetrical Parkinsonism, coarse postural tremor and presence of:
- Orolingual dyskinesias
- Tardive dystonia
- Akathisia (feeling of inner restlessness)
are signs of what?

A

Drug-induced Parkinsonism

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138
Q

What is the frequency of an essential tremor?

A

Up to 12Hz

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139
Q

What is the typical cause of an essential tremor?

A

Autosomal dominant inheritance

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140
Q

What is the usual age of onset of an essential tremor?

A

15 years

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141
Q

When does multi-system atrophy tend to onset?

A

6th or 7th decade

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142
Q

What is the core triad of features of Multi-System Atrophy?

A

Dysautonomia
Cerebellar features
Parkinsonism

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143
Q

What sort of tremor is seen in Multi-System Atrophy?

A

Jerky postural

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144
Q

What pyramidal signs are seen in Multi-System Atrophy?

A

Hyperreflexia

Babinski positive

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145
Q

What other signs are seen in Multi-System Atrophy?

A

Severe dysarthria or dysphonia
Marked antecollis (excessive forward neck flexion)
Inspiratory sighing
Orofacial dystonia

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146
Q

What might an MRI in Multi-System Atrophy show?

A

“Hot cross bun signs”:

  • Cerebellar and pontine atrophy
  • Hyperintense rim around putamen in T2 MRI
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147
Q

What gaze is typically affected in Progressive Supranuclear Palsy?

A

Vertical

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148
Q

What signs/symptoms are seen in Progressive Supranuclear Palsy?

A 
Symmetric akinetic-rigid syndrome (mainly axial)
Poor gait and balance - Early falls
Pseudobulbar symptoms
Retrocollis
Staring (continuous frontalis activity)
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149
Q

What sort of response does Progressive Supranuclear Palsy have to levopdopa?

A

None

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150
Q

What causes Fragile X-Tremor Ataxia Syndrome?

A

Abnormal number of CGG repeats in FMR1 gene:

- In the range of 55-200

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151
Q

What are the core symptoms of Fragile X-Tremor Ataxia Syndrome?

A 
Cerebellar gait ataxia
Postural/Intention tremor
Variable Parkinsonism
Dysuatonomia
Frontal cognitive decline
Peripheral neuropathy
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152
Q

What is the typical age of onset of Fragile X-Tremor Ataxia Syndrome?

A

> 50 years

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153
Q

How does Fragile X-Tremor Ataxia Syndrome tend to present in women?

A

Milder:

  • Premature ovarian failure
  • Early menopause
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154
Q

What MRI signs are seen in Fragile X-Tremor Ataxia Syndrome?

A

T2 hyperintensities in middle cerebral peduncles

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155
Q

What hyperkinetic movement disorder is a tremor?

A

Rhythmic sinusoidal oscillation of a body part

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156
Q

What hyperkinetic movement disorder is a tic?

A

Involuntary stereotyped:

  • Movements OR
  • Vocalisations
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157
Q

What hyperkinetic movement disorder is chorea?

A

Brief, irregular purposeless movements

Movements flow from one body part to another

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158
Q

What hyperkinetic movement disorder is myoclonus?

A

Brief ‘electric-shock’ like jerks

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159
Q

What hyperkinetic movement disorder is dystonia?

A

Abnormal posture of affected body part

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160
Q

What typically causes a resting tremor?

A

Parkinson’s
Drug-induced Parkinsonism
Psychogenic tremor

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161
Q

What typically causes a postural tremor?

A

Essential tremor
Enhanced physiological tremor
Tremor associated with neuropathy

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162
Q

What causes a kinetic tremor?

A

Cerebellar disease:

  • Demyelination
  • Haemorrhage
  • Degenerative
  • Toxic (eg. alcohol)
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163
Q

What can cause a head tremor?

A

Dystonia

Cerebellar disease

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164
Q

What can cause a jaw tremor?

A

Dystonia

Parkinson’s disease

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165
Q

What can cause a palatal tremor?

A

Ataxia
Symptomatic
Essential tremor

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166
Q

If a tremor is present in yonger people (<45 years) what should be considered and how do we investigate?

A

Wilson’s Disease:

  • Copper
  • Caeruloplasmin
167
Q

What is the first line treatment for a dystonic tremor (including essential tremor)?

A

Propanolol
OR
Primidone

168
Q

What are some secondary options for treatment of dystonic/essential tremor?

A

Atenolol
Gabapentin
Topiramate
Clonazepam

169
Q

Is severely affected by a dystonic/essential tremor, what treatment can be offered?

A

Deep brain stimulation

170
Q

What are primary dystonic syndromes?

A

Dystonia-Plus syndromes:

  • Dopamine responsive dystonia
  • Myoclonic dystonia
171
Q

What are secondary dystonic syndromes?

A

Symptomatic
Heredodegenerative:
- Wilson’s Disease
- Parkinson’s Disease

172
Q

What is the age at which a dystonic syndrome would be consider young-onset?

A

<28 years

173
Q

What parts of the brain are usually affected in dystonia?

A

Basal ganglia:

  • Putamen
  • Globus pallidus
174
Q

What are the three main phsyiological abnormalities in dystonia?

A

Loss/Reduction in reciprocal inhibition
Alterations in brain plasticity
Alterations in sensory function

175
Q

What causes torsion dystonia?

A

DYT1 mutations

176
Q

When does torsion dystonia usually onset?

A

<28 years (usually childhood)

177
Q

Where does torsion dystonia usually start?

A

Lower limb (usually legs)

178
Q

How long does it take for torsion dystonia to progress to generalised/multifocal dystonia?

A

5-10 years

179
Q

What inheritance is torsion dystonia?

A

Autosomal dominant

180
Q

How can cervical dystonia be treated?

A

Botox A or B

181
Q

What is the procedure of choice in treating dystonia?

A

Deep brain stimulation

182
Q

What inherited/degenerative disorders can cause chorea?

A 
Huntington's Disease
Wilson's Disease
Neuroacanthocytosis
Benign Hereditary CHorea
Ataxia Telangiectasia
Spinocerebellar Ataxia Type 17
183
Q

What infection can cause chorea?

A

HIV

184
Q

What disease can display paroxysmal chorea?

A

Parkinson’s Disease

185
Q

What are some other causes of chorea?

A 
Autoimmune
Metabolic
Drugs:
- Dopamine receptor blockers
- Levopdopa
- COC
186
Q

How can chorea be treated?

A

Treat underlying cause
Symptomatic treatment:
- Terabenazine
- Dopamine receptor antagonists

187
Q

What is the mode of inheritance of Huntington’s Disease?

A

Autosomal dominant

188
Q

What is Huntington’s Disease characterised by?

A

Progressive behavioural disturbance
Dementia
Movement disorder - Usually chorea

189
Q

What is the M:F ratio in Huntingtons?

A

Equal

190
Q

Where are high prevalence populations for Huntingtons

A 
Moray Forth (Scotland)
Venezuela
191
Q

Where are there low rates of Huntington’s?

A

Japan

African Americans

192
Q

What is the usual age of onset of Huntington’s?

A

4th decade

193
Q

What is the genetic mutation in Huntington’s?

A

CAG triplet-repeat expansion disorder:

  • Affects Huntingtin gene on chromosome 4
  • Usually 20 in normal individuals (codes of glutamine)
194
Q

How many repeats of the gene mutation must be present for Huntington’s to definitely occur?

A

> =40

195
Q

How many repeats of the gene mutation must be present to ensure Huntington’s does not occur?

A

=<35

196
Q

What is copropraxia?

A

Obscene gestures

197
Q

What is echopraxia?

A

Copying others’ movements

198
Q

What is coprolalia?

A

Obscene words

199
Q

What is echolalia?

A

Copying others’ words

200
Q

What is palilalia?

A

Repetition of the same word/phrase/syllable

201
Q

When do primary tic disorders tend to start?

A

Childhood

202
Q

What psychopathology may be associated with tics?

A

OCD
ADHD
Anxiety
Self-harm

203
Q

What investigations are important in tics?

A

Copper
Blood for acanthocytosis
ASO titres
Uric acid

204
Q

What developmental disorders can cause tics?

A

Down syndrome
Fragile X syndrome
Autism

205
Q

What structural abnormalities can cause tics?

A

Post-encephalopathy

Basal ganglia lesions (usually caudate nucleus)

206
Q

What infections can cause tics?

A

Sydenham’s Chorea (with rheumatic fever)

Paediatric Autoimmune Neuropsychiatric Disorders Associated with Strep. (PANDAS)

207
Q

What drugs and toxins can cause tics?

A

CO poisoning
Cocaine
Amphetamines
Anticonvulsants

208
Q

What is the diagnostic criteria for Tourette Syndome?

A 
Both of:
- Multiple motor tics
- >= 1 vocal tics
Tics must occur:
- Many times a day
- Nearly every day OR
- Intermittently for >= 1 year with <=3 months intervals of being tic-free
Age of onset <= 18 years
Exclusion of obvious secondary cause
209
Q

What is the symptomatic treatment of the tics in Tourette?

A

Clonidine

Tetrabenazine

210
Q

What is an example of negative myoclonus?

A

Asterixis (liver flap)

211
Q

What are causes of myoclonus plus dementia?

A

Alzheimer’s
Lewy Body dementia
Creutzfeldt-Jakob Disease

212
Q

What are causes of myoclonus plus Parkinsonism?

A

Corticobasal degeneration
Multiple System Atrophy
Spinocerebellar ataxias

213
Q

What typically precipitates juvenile myoclonus epilepsy?

A

Alcohol

Sleep deprivation

214
Q

When are symptoms worst in juvenile myoclonus epilepsy?

A

In the morning

215
Q

How is juvenile myoclonus epilepsy treated?

A

Sodium valproate

Levetiracetam

216
Q

What drug can aggravate juvenile myoclonus epilepsy?

A

Carbamazepine

217
Q

When glutamate and aspartate are released in a head injury, what happens that increases the damage?

A 
Intracelluar calcium release
Phospholipase activation
Breakdown of cell membrane:
- Cell swelling
- Apoptosis
218
Q

What do the loss of the BBB and leucocyte infiltration cause in head injury?

A

Secondary inflammation

219
Q

What does the loss of cerebral autoregulation of BP cause in head injury?

A

Secondary ischaemia

220
Q

What does the loss of cerebral autoregulation of blood flow cause in head injury?

A

Metabolic de-coupling:

- Even more ischaemia and oedema

221
Q

What is the equation for cerebral perfusion pressure?

A

CPP = MAP - ICP

222
Q

What CPP do we aim for in head injury?

A

> 60 mmHg

223
Q

What is normal adult ICP?

A

9-11 mmHg (12-15 cm H2O)

224
Q

What is a common sign in anterior cranial fossa fracture?

A

‘Raccoon’ or ‘Panda’ eyes

225
Q

What is a common sign in middle cranial fossa fracture?

A

‘Battle signs’ over mastoid

226
Q

What focal signs can be present in head injury?

A

Lateralising motor signs

CN iii palsy (pupillary light reflex)

227
Q

What is a subfalcine herniation?

A

Frontal lobe scraped under falx cerebri

228
Q

What is the first sign of a subfalcine herniation?

A

Leg weakness

229
Q

What is a transtentorial (uncal) herniation?

A

Temporal lobe herniates and presses against brainstem and CN iii

230
Q

What are the first signs of a transtentorial (uncal) herniation?

A 
Coma (brainstem compression)
Pupil dilatation (reduced PNS supply via CN iii)
231
Q

What is tonsillar herniation?

A

‘Coning’

Cerebellum herniates through foramen magnum and presses against brainstem

232
Q

What are the signs in tonsillar herniation?

A

BP collapses
Cardiac arrest
Both result in death

233
Q

What are the ‘eye’ scores in the GCS?

A

Spontaneously open = 4
Open to command = 3
Open to pain = 2
None = 1

234
Q

What are the verbal response scores in the GCS?

A 
Orientated = 5
Confused = 4
Inappropriate words = 3
Incomprehensible sounds = 2
None = 1
235
Q

What are the motor response scores in the GCS?

A 
Obeys commands = 6
Localises pain = 5
Flexion in response to pain = 4
Decorticate posturing (abnormal flexion) = 3
Decerebrate posturing (extension) = 2
None = 1
236
Q

What is the definition of coma?

A

Doesn’t open eyes
Doesn’t obey commands
Doesn’t speak

237
Q

What GCS score indicates coma?

A

=<8

238
Q

What kills a patient in head trauma?

A

Hypoxia
Hypotension
Increased ICP

239
Q

How long after cardiovascular arrest does irreversible brain damage occur?

A

5 minutes

240
Q

When should a CT be requested in head trauma?

A

A skull fracture OR
Not orientated (GCS <15) OR
With focal neurological signs OR
Taking anticoagulants (warfarin)

241
Q

How does sedation help in head trauma?

A

Reduces cerebral metabolic rate
Reduces cerebral blood flow
Reduces ICP

242
Q

How can we improve micro-circulation in head injury?

A

Mannitol
OR
Hypertonic saline

243
Q

When is epilepsy most common following a head injury?

A

In the first 2 weeks

244
Q

Where can CSF leak into following a head injury?

A

Nose

Ear

245
Q

Poor concentration, headache, poor memory and lethargy following a head injury are signs of what?

A

Post-concussion syndrome

246
Q

How many patients are affected by cognitive problems following a head injury?

A

30%

247
Q

How is Duchenne Muscular Dystrophy inherited?

A

X-linked recessive

248
Q

Where is the mutation in Duchenne Muscular Dystrophy?

A

Xp21

249
Q

What is the incidence in males of Duchenne Muscular Dystrophy?

A

1/3000

250
Q

When and where does the weakness onset in Duchenne Muscular Dystrophy?

A

3-4 years of age

Pelvic and shoulder girdles

251
Q

At what age do most Duchenne Muscular Dystrophy patients become wheelchair bound?

A

10-12 weeks

252
Q

What spinal feature is characteristic in Duchenne Muscular Dystrophy?

A

Lumbar hyperlordosis

253
Q

What muscles hypertrophy in Duchenne Muscular Dystrophy? How are they often described?

A

Calf muscles

‘Woody’

254
Q

What is deficient in Duchenne Muscular Dystrophy?

A

Dystrophin

255
Q

70% of Duchenne Muscular Dystrophy patients have what genetic abnormality?

A

Large scale deletions of dystrophin gene

256
Q

30% of Duchenne Muscular Dystrophy patients have what genetic abnormality?

A

Point mutations

Small insertions and deltions

257
Q

What is Gower’s sign?

A

Indicates proximal muscle weakness

Patients have to ‘walk’ themselves up from sitting with their hands and arms

258
Q

What investigations suggest Duchenne Muscular Dystrophy?

A

Raised serum CK
EMG
Muscle biopsy

259
Q

What are some differentials for Duchenne Muscular Dystrophy?

A

Autosomal recessive limb girdle muscular dystrophies:

- Some due to sarcoglycan deficiencies

260
Q

What is the incidence of Huntington’s Disease?

A

1/20000

261
Q

What are the early clinical signs of Huntington’s Disease?

A 
Clumsiness
Agitation
Apathy
Anxiety
Abnormal eye movements
Depression
262
Q

What macroscopic change is seen in Huntington’s Disease?

A

Caudate nucleus atrophy

263
Q

What percentage of cases of dementia are due to Alzheimer’s Disease?

A

50-70%

264
Q

What is the pathophysiology of Alzheimer’s Disease?

A

Loss of cortical neurones
Intracellular neurofibrillay tangles
Extraceullar senile plaques

265
Q

What are the extracellular protein deposits in Alzheimer’s Disease?

A

Amyloid beta protein

266
Q

Where are the extracellular protein deposits seen in Alzheimer’s Disease formed from?

A

Fragments of the product of the amyloid precursor protein gene (Chromosome 21)

267
Q

How does an autosomal dominant form of Alzheimer’s Disease affect the age of onset?

A

Earlier

268
Q

When is the onset of Alzheimer’s Disease in Dowrr Syndome?

A

3rd or 4th decde

269
Q

What mutations can result in Alzheimer’s Disease?

A 
APP mutations (Chromosome 21)
Presenilin 1 (Chromosome 14)
Presenilin 2 (Chromosome 1)
270
Q

Where are glial cells derived from?

A

Neuroectoderm

271
Q

Where are microglia derived from?

A

Mesoderm

272
Q

Where do microglia originate?

A

Bone marrow

273
Q

What cells does hypoxic damage to the CNS affect most

A

Neurones

274
Q

How does hypoxia damage cells in the CNS

A

Activation of glutamate receptors
Uncontrolled calcium influx
Neurones can use anaerobic glycolysis

275
Q

The following are signs of what sort of injury:

  • Increased RNA and protein synthesis
  • Cell body swelling
  • Peripheral displacement of nucleus
  • Enlargement of nucleolus
  • Central chromatolysis
  • Anterograde degeneration
  • Breakdown of myelin
A

Axonal injury

276
Q

What is gliosis?

A

Reactive response associated with prolifetation

277
Q

What does gliosis result in?

A

Cell death

Degeneration

278
Q

What is the most important histological indicator of CNS injury?

A

Gliosis

279
Q

What do astrocytes undergo in gliosis?

A

Hyperplasia

Hypertrophy

280
Q

What happens to nuclei in gliosis?

A

Enlarge

Become vesicular

281
Q

How does the cytoplasm appear in gliosis?

A

Bright pink
Irregular
Swathes around oddly placed nucleus

282
Q

What are glial fibrils?

A

Extension of ramifying processes of cytoplasm

283
Q

What is cytoplasmic expansion in gliosis associated with?

A

Increased production of glial fibrillay acidic protein

284
Q

What happens in old gliosis lesions?

A

Nuclei become small and dark

Nuclei lie in dense net of glial fibrils

285
Q

How does gliotic tissue appear?

A

Translucent and firm

286
Q

What are microglial nodules?

A

Microglia forming aggregates about foci of necrosis

287
Q

What are neuronophagia?

A

Microglial congregations around portions of dying neurones

288
Q

What percentage of cardiac output does the brain receive?

A

15%

289
Q

How much of the oxygen in the body does the brain consume?

A

20%

290
Q

How does the brain get ATP?

A

Active aerobic metabolism of glucose

291
Q

What happens to the vasculature in the brain in response to hypertension?

A

Constricts

292
Q

What is Weber’s syndrome?

A

Vertebrobasilar pathology affecting the midbrain:

  • Ipsilateral CN iii palsy
  • Contralateral hemiparesis/hemiplagia
293
Q

What is Global Hypoxic-Ischaemic Encephalopathy?

A

Parenchymal injuries with generalised decrease in blood flow

294
Q

When does cerebral autoregulation fail?

A

When systolic BP <50 mmHg

295
Q

What does mild ischaemic result in?

A

Preferential loss of selectively vulnerable neurones

296
Q

What does moderate ischaemic result in?

A

Selective neuronal necrosis

Glial and endothelial cells preserved

297
Q

What does complete ischaemia result in?

A

Pan-necrosis

298
Q

What groups of neurones are most vulnerable to hypoxic-ischaemic damage?

A

Pyramidal cells of hippocampus
Purkinje cells of cerebellum
Those within globus pallidus

299
Q

What are the ‘watershed areas’?

A

Junctions of arterial territories

300
Q

Where do the ‘watershed areas’ receive blood from?

A

Dual supply from most distal arterial branches

301
Q

What affects the ‘watershed areas’ first?

A

Hypotension

302
Q

Give examples of ‘watershed areas’.

A

Superior cerebral convexities:
- Ant. and Middle cerebral artery junctions
Posterior cerebellum:
- Ant. and Post. cerebellary artery junctions

303
Q

What are the signs/symptoms of hypoxic-ischaemic encephalopathy?

A

Arrhythmias
Shock
Increased ICP

304
Q

What age is the peak incidence of cerebral infarction?

A

70+ years

305
Q

Where does thrombosis most commonly occur in cerebral infarction?

A

Bifurcation of common carotids

306
Q

Where do most emboli arise in cerebral infarction?

A

Heart

Atherosclerotic plaques in more proximal arteries

307
Q

Where do most emboli occlusions occur in cerebral infarction?

A

Middle cerebral arteries

308
Q

Apart from thrombosis and emboli, what else can cause occlusion?

A

Vasculitis

Trauma

309
Q

What causes of cerebral infarction does atheroma increase the risk of?

A

Basilar artery (usually);

  • Thrombosis
  • Aneurysm
310
Q

How can hypertension result in cerebral infarction?

A

Atherosclerosis of small penetrating vessels:

- Muscle in walls replaced with hyaline (weaker)

311
Q

What infarcts does hypertension result in?

A

Lacunar infarcts

312
Q

At what time do ischaemic neuronal changes occur in CVA?

A

5 to 20 hours

313
Q

When does inflammation and extravasation of RBCs occur in CVA?

A

24 to 36 hours

314
Q

At what time are necrotic areas following CVA visible macroscopically?

A

36 to 48 hours

315
Q

What happens on day 3 following a stroke?

A

Macrophages infiltrate:

  • Phagocytose necrotic debris
  • Sharper demarcation of site of infarction
316
Q

What happens in the 1st-2nd week following CVA?

A

Liquefaction of tissue and gliosis (Colliquative necrosis)

317
Q

What happens a few months after a CVA?

A

Cavitation

Completion of glial scar

318
Q

Spontaneous saccular aneurysm rupture is more common in what sex?

A

Female

319
Q

What conditions increase the incidence of Berry aneurysms?

A 
PKD
Fibromuscular dysplasia
Coarctation of arota
Arteriovenous malformations in the brain
Collage iii developmental abnormality
320
Q

Where do most saccular aneurysms arise?

A

Bifurcations (in internal carotid territory)

321
Q

At what size are saccular aneurysms at greatest risk of rupture?

A

6-10cm

322
Q

At what size do saccular aneurysms loss most risk of rupture but cause symptoms due to mass effect?

A

> =25cm

323
Q

Why may parenchymal infarcts develop after an aneurysm rupture?

A

Arterial spasm
Mass effect due to:
- Haematoma
- Increased ICP

324
Q

What symptoms is a subarachnoid haemorrhage associated with?

A

Severe headache
Vomiting
Loss of consciousness

325
Q

In what sex are subarachnoid haemorrhages most common?

A

Female

326
Q

How does the CSF appear in a subarachnoid haemorrhage?

A

Bloody

327
Q

What can cause chronic hydrocephalus following a subarachnoid haemorrhage?

A

Organisation of blood in:
- Leptomeninges
- Arachnoid granulations
CSF flow obstruction

328
Q

What substance is myelin rich in?

A

Phospholipid

329
Q

What are metabolic causes of secondary demyelination?

A

Progressive Multifocal Leucoencephalopathy

Contral Pontine Myelinosis

330
Q

What infections can cause secondary demyelination?

A

Sub-acute Sclerosing Panencephalitis:
- Post measles complication (1/10000)
AIDS

331
Q

What toxins can cause secondary demyelination?

A

Low-grade, non-fatal cyanide
CO (chronic, low-levels)
Solvents

332
Q

What is the M:F ratio of MS?

A

1:2

333
Q

What is the prevalence of MS?

A

1/1000

334
Q

What is the defining feature of MS?

A

Episodes of neurological deficit separated by time and space

335
Q

How does MS appear on a T1 weighted MRI?

A

Hypointense

336
Q

How does MS appear on a T2 weighted MRI?

A

Hyperintense

337
Q

What is one of the earliest clinical signs and is often the first sign at presentation in MS?

A

Optic neuritis

338
Q

Apart from visual disturbance, what are some other common manifestations in MS?

A

Paraesthesia
Spasticity
Speech disturbance
Gait abnormalities

339
Q

What vitamin might be related to MS?

A

Vitamin D

340
Q

Why does the external surface of the brain appear normal in MS?

A

Grey matter has no myelin

341
Q

On a cut surface of the brain, how do the demyelinated plaques appear?

A

Well-demarcated
Soft and pink in acute lesions
Firmer and pearly grey

342
Q

Where are plaques common in MS?

A

CN ii and optic tract
Periventricular white matter
Corpus callosum
Brainstem and spinal cord

343
Q

Where are acute MS plaques often centred around?

A

Veins

344
Q

Why are chronic inactive MS plaques well-defined?

A

Astrocytic proliferation and gliosis are prominent

345
Q

Where are chronic inactive MS plaques classically located?

A

Around lateral ventricles

346
Q

What are shadow plaques in MS?

A

Plaques were the border between normal and affected white matter is ill-defined

347
Q

What cells typically result in inflammation in MS?

A

Lymphocytes (T cells)

348
Q

What type of glia are most common in MS gliosis?

A

Astrocytes

349
Q

What metabolic conditions can result in secondary dementia?

A

Uraemia

Hepatic failure

350
Q

What conditions associated with paraneoplastic syndromes can commonly cause secondary dementias?

A

Small-cell lung cancer

Some squamous cell carcinomas

351
Q

What is Biswanger’s Disease?

A

Vascular dementia due to white matter damage in hypertension

352
Q

In what genetic condition is the risk of Alzheimer’s Disease increased?

A

Down’s Syndrome

353
Q

How does Alzheimer’s Disease tend to present?

A

Insidious impairment of higher functions:

  • Mood
  • Behaviour
354
Q

What are some later signs of Alzheimer’s Disease?

A

Disorientation
Memory loss
Aphasia

355
Q

What do the later signs of Alzheimer’s Disease indicate?

A

Severe cortical dysfunction

356
Q

What macroscopic pathologies are seen in Alzheimer’s Disease?

A

Marked decreased in brain size (cortical atrophy)
Widening of sulci
Narrowing of gyri
Secondary hydrocephalus (ventricular dilatation)

357
Q

What lobe of the brain is often spared in Alzheimer’s Disease?

A

Occipital

358
Q

What is the main component of intracytoplasmic neurofibrillay tangles in Alzheimer’s Disease? Why is it pathological?

A

Tau protein:

- Abnormally phosphorylated

359
Q

What effect do intracytoplasmic neurofibrillay tangles have on the cell?

A

Displace/Encircle nucleus

360
Q

What is the main component of the extraceullar senile/neuritic plaques in Alzheimer’s Disease? What is this cleaved to?

A

A-beta amyloid plaques:

- Cleaved to beta-pleated sheet

361
Q

Where are extracellular senile/neuritic plaques most common in Alzheimer’s Disease?

A

Hippocampus
Cerebral cortex
Deep grey matter

362
Q

Where is there excessive neuronal loss with astrocytosis in Alzheimer’s Disease?

A

Hippocampus
Frontal lobe
Temporal lobe

363
Q

What cells accumulate in amyloid?

A

Eosinophils

364
Q

How does amyloid stain? What stain is used?

A

Congo Red stain:

- Bright apple-green

365
Q

On electron microscopy, how big is amyloid?

A

10-12nm fibrils

366
Q

What are the hallmarks of Lewy Body Dementia?

A

Progressive dementia with:

  • Hallucinations
  • Fluctuating attention
  • Parkinsonism
367
Q

What do Lewy Bodies produce?

A

Ubiquitin

368
Q

Where is the Huntingtin gene located?

A

Chromosome 4p16.3

369
Q

What is Pick’s Disease?

A

Progressive dementia characterised by:

- Changes in character and social deterioration

370
Q

When does Pick’s disease usually present?

A

50-60years

371
Q

What does Pick’s Disease lead to?

A

Impaired:

  • Intellect
  • Memory
  • Language
372
Q

What are the macroscopic changes in Pick’s Disease?

A

Extreme atrophy of temporal and frontal lobes

373
Q

How much does the brain weight in Pick’s Disease?

A

<1kg

374
Q

What are the microscopic changes in Pick’s Disease?

A

Neuronal loss and astrocytosis
Pick’s cells (Swollen neurones)
Pick’s bodies (Intracytoplasmic filamentous inclusions)

375
Q

How quickly does Pick’s Disease progress?

A

Rapidly:

- 2-10 years from diagnosis to death (mean is 7)

376
Q

Why does multi-infarct dementia often result in anxiety and depression?

A

Sufferers are aware of their deficits

377
Q

What signs suggest multi-infarct dementia?

A

Abrupt onset
Stepwise progression
PMHx of hypertension and CVA
CT/MRI evidence of CVA

378
Q

When does a diffuse axonal injury occur

A

At moment of injury

379
Q

Where is the most common location of diffuse axonal injury?

A

Brainste,

380
Q

What cells appear and where weeks after a diffuse axonal injury?

A

Clusters of microglia in white matter

381
Q

What occurs in the 2-4 hours following a diffuse axonal injury?

A

Focal APP accumulation impairing axonal transport

382
Q

What occurs in the 12-24 hours following a diffuse axonal injury?

A

Axonal varicosity -> Axonal swelling -> Brain swelling

383
Q

What does calcium influx in diffuse axonal injury result in?

A

Activation of calpains
Cytoskeletal disruption
Disrupted antegrade flow

384
Q

If an epidural haemorrhage goes untreated, what can happen?

A

Midline shift:

  • Compression
  • Herniation
385
Q

What is a subfalcine herniation associated with?

A

Anterior cerebral artery compression

386
Q

What type of respiration can result from herniation?

A

Cheyne-Stokes:

  • Progressively deeper
  • Sometimes faster
387
Q

In what people are abscesses common?

A

IVDUs

388
Q

What sort of cerebral oedema is due to:
- Defects in BBB
- Water, sodium and protein leak into extracellular space
Where does it occur?

A

Vasogenic

White matter

389
Q

What is the commonest cause of cytotoxic cerebral oedema?

A

Ischaemia

390
Q

What causes hydrostatic cerebral oedema?

A

Low protein
Fluid flows into extracellular space -> Supped increase in ICP
Dilatation of capillary bed

391
Q

In what condition is hydrostatic cerebral oedema seen?

A

Hypertensive encephalopathy

392
Q

What type of cerebral oedema results from fluid forced into paraventricular white matter?

A

Interstitial

393
Q

In what type of haemorrhage might patients experience a lucid interval before losing consciousness?

A

Epidural

394
Q

Why are gyrud contours preserved in subdural haemorrhage?

A

Pressure is evenly distributed (unlike in an epidural haemorrhage)

395
Q

Why is symptom onset of a subdural haemorrhage often slower?

A

Venous bleed

396
Q

What typically causes chronic subdural haemorrhages?

A

Brain atrophy - Bridging veins become more vulnerable

397
Q

What is the composition of a chronic subdural haemorrhage?

A

Liquefied blood:

  • Yellowish
  • Separated from brain by neomembrane
398
Q

What contrast agents can be used in brain CT?

A

Niopam
Ultravist
Ominoaque

399
Q

When do we take the scan to receive a CT angiogram?

A

During and immediately after bolus is pumped in

400
Q

When do we take a scan to receive a CT venogram?

A

30 seconds later

401
Q

After how long with a CT scan show enhancement where there has been BBB disruption (eg in tumours and inflammation)?

A

5 minutes

402
Q

What substances can be used as contrast in MRI?

A

Paramagnetic (eg. Gadolinium):

  • Magnevist
  • Dotarem
403
Q

What are the indications for angiography?

A

Investigation of spontaneous subarachnoid haemorrhage
Suspected aneurysm/AVM
Carotid stenosis

404
Q

Where will blood be present on CT in a subarachnoid haemorrhage?

A

Ventricles
Sylvian fissures
Basal cisterns
Surface subarachnoid space

405
Q

What is the gold standard investigation into a subarachnoid haemorrhage?

A

Digital subtraction angiography

406
Q

What shows up as hyperintense on a T1 MRI?

A

Fat and the 4 Ms:

  • Methaemoglobin
  • Mineral deposition
  • Melanin
  • “Mush” (highly proteinaceous fluid)
407
Q

What shows up as hypointense on T1 MRI?

A

Water
Air
Cortical bone
High flow (Arterial “flow voids”)

408
Q

What shows up as hyperintense on a T2 MRI?

A 
Water (less tissue = more water):
- Fluid collection
- Oedema
- Demyelination
- Gliosis
- Some tumours
Fat (although it is usually suppressed)
409
Q

What shows up as hypointense on a T2 MRI?

A

Some blood products (sub-acute haematoma)
Minerals
Air and bone
High flow

410
Q

What is N-acetyl aspartate a marker of?

A

Neuronal density and neurometabolic fitness

411
Q

What is N-acetly aspartate correlated to?

A

Rate of mitochondrial phosphorylation

412
Q

What is the “Cho” peak formed of in MR spectroscopy?

A

Choline
Ach
Glycerophorycholine
Phosphocholine

413
Q

What is the “Cr” peak formed of in MR spectroscopy?

A

Creatinine

Phosphocreatinine

Year 3 - Neurology (DP) (5 decks)

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