Neurologie Flashcards
(135 cards)
1
Q
What is the onset type of delirium?
A
Acute onset
2
Q
List some motor signs associated with delirium.
A
- Tremor
- Myoclonus
- Asterixis
3
Q
What speech characteristic is commonly observed in delirium?
A
Slurred speech
4
Q
Describe the types of altered consciousness seen in delirium.
A
- Hyperalert/agitated
- Lethargic
- Fluctuations
5
Q
What type of hallucinations may occur in delirium?
A
Florid hallucinations
6
Q
What EEG finding is characteristic of delirium?
A
Pronounced diffuse slowing
7
Q
What is classic migraine?
A
Common migraine + aura. May have H/A with occasional focal neurologic deficit(s) that resolve completely in ≤ 24 hrs.
H/A stands for headache.
8
Q
What is the most common type of transient neurologic disturbance in classic migraine?
A
Visual disturbances
Over half of the transient neurologic disturbances are visual.
9
Q
What are examples of positive phenomena in visual disturbances associated with classic migraine?
A
- Spark photopsia
- Stars
- Complex geometric patterns
- Fortification spectra
These phenomena may precede negative phenomena.
10
Q
What are some negative phenomena that may occur after positive phenomena in classic migraine?
A
- Scotoma
- Hemianopia
- Monocular or binocular visual loss
Negative phenomena may follow visual disturbances.
11
Q
What is the second most common type of symptom in classic migraine?
A
Somatosensory disturbances involving the hand and lower face
These symptoms are less frequent than visual disturbances.
12
Q
List some less common deficits that may occur in classic migraine.
A
- Aphasia
- Hemiparesis
- Unilateral clumsiness
These deficits are less frequently observed.
13
Q
What is characteristic of the progression of deficits in classic migraine?
A
A slow march-like progression
This progression is a notable feature of neurologic deficits in classic migraine.
14
Q
What is the risk associated with migraine patients?
A
Increased risk of stroke
This risk is considered probable in patients with migraine.
15
Q
What are the three components of the classic triad of Parkinson’s disease?
A
- Tremor (resting, 4–7/second)
- Rigidity (cogwheel)
- Bradykinesia
The classic triad refers to the most common symptoms observed in individuals with Parkinson’s disease.
16
Q
What is the underlying cause of Parkinsonism?
A
Relative loss of dopamine mediated inhibition of acetylcholine effects in the basal ganglia
This neurochemical imbalance leads to motor symptoms characteristic of Parkinsonism.
17
Q
What is the primary degeneration observed in Parkinson’s disease?
A
Degeneration of pigmented dopaminergic neurons in the pars compacta of the substantia nigra
18
Q
What type of neurons are primarily affected in Parkinson’s disease?
A
Pigmented (neuromelanin-laden) dopaminergic neurons
19
Q
Which area of the brain shows reduced levels of dopamine in Parkinson’s disease?
A
Neostriatum
20
Q
What are the components of the neostriatum where dopamine levels are reduced?
A
- Caudate nucleus
- Putamen
- Globus pallidus
21
Q
True or False: Parkinson’s disease is characterized by increased levels of dopamine in the brain.
A
False
22
Q
Fill in the blank: Degeneration of pigmented dopaminergic neurons leads to reduced levels of _______ in the neostriatum.
A
dopamine
23
Q
What is Multiple System Atrophy (MSA) also known as?
A
Shy-Drager syndrome
24
Q
What are the key characteristics of MSA?
A
Parkinsonism, idiopathic orthostatic hypotension, signs of autonomic nervous system dysfunction
25
What type of dysfunction may precede parkinsonism in MSA?
Autonomic nervous system dysfunction
26
List some findings associated with autonomic nervous system dysfunction in MSA.
* Urinary sphincter disturbance
* Hypersensitivity to noradrenaline infusions
* Hypersensitivity to tyramine infusions
27
What part of the nervous system is affected in MSA?
Preganglionic lateral horn neurons of thoracic spinal cord
28
True or False: Most patients with MSA respond to dopa therapy.
False
29
Fill in the blank: MSA is characterized by parkinsonism indistinguishable from _______.
Idiopathic paralysis agitans (IPA)
30
What is another name for Progressive Supranuclear Palsy?
Steele-Richardson-Olszewski syndrome
## Footnote
This condition is characterized by specific neurological symptoms.
31
What are the three main components of the triad associated with Progressive Supranuclear Palsy?
* Progressive supranuclear ophthalmoplegia
* Pseudobulbar palsy
* Axial dystonia
## Footnote
Each component represents a distinct set of symptoms related to the disorder.
32
Define progressive supranuclear ophthalmoplegia in the context of Progressive Supranuclear Palsy.
Paresis of voluntary vertical eye movement, but still moves to vertical doll's eyes maneuver
## Footnote
This condition primarily affects the ability to move the eyes vertically.
33
What symptoms are associated with pseudobulbar palsy in Progressive Supranuclear Palsy?
* Mask-like facies
* Marked dysarthria
* Dysphagia
* Hyperactive jaw jerk
* Emotional incontinence (usually mild)
## Footnote
These symptoms reflect the involvement of cranial nerves and emotional regulation.
34
What type of dystonia is particularly noted in Progressive Supranuclear Palsy?
Axial dystonia, especially of neck and upper trunk
## Footnote
This type of dystonia can lead to abnormal postures and movements.
35
What is multiple sclerosis?
An idiopathic demyelinating disease of the CNS producing exacerbating and remitting symptoms disseminated in space and time
## Footnote
Multiple sclerosis (MS) is characterized by periods of symptom flare-ups and remissions.
36
What are classic clinical findings of multiple sclerosis?
Optic neuritis, paresthesias, INO (internuclear ophthalmoplegia), and bladder symptoms
## Footnote
These symptoms are commonly associated with MS and can vary among patients.
37
What do the diagnostic criteria for multiple sclerosis use?
Clinical and/or lab results (MRI, CSF…) to stratify patients as: MS, probable MS, or not MS
## Footnote
This stratification helps in determining the appropriate diagnosis and treatment approach.
38
What and where does MRI reveal in multiple sclerosis?
Multiple usually enhancing lesions involving optic nerves & white matter of brain, cerebellum, and spinal cord
## Footnote
Enhancing lesions on MRI indicate active inflammation in the CNS.
39
Fill in the blank: The classic clinical findings of multiple sclerosis include optic neuritis, ________, INO, and bladder symptoms.
paresthesias
40
True or False: The McDonald criteria are used to diagnose multiple sclerosis.
True
41
What is the significance of disseminated symptoms in multiple sclerosis?
They indicate the presence of the disease affecting multiple areas of the CNS over time
## Footnote
This characteristic is essential for the diagnosis of MS.
42
43
What were the only considerations in the study regarding laboratory support?
CSF oligoclonal bands (CSF-OCB) or increased CSF IgG production
## Footnote
OCB must not be present in serum
44
What does CSF-OCB stand for?
Cerebrospinal fluid oligoclonal bands
45
True or False: OCB must be present in serum for the study's laboratory support.
False
46
Fill in the blank: Increased _______ production is a consideration for laboratory support in the study.
CSF IgG
47
What is the full form of ADEM?
Acute disseminated encephalomyelitis
48
What does ADEM stand for?
Acute disseminated encephalomyelitis
49
What are motor neuron diseases?
Degenerative diseases of motor neurons
50
What is the most common subtype of degenerative motor neuron diseases?
Amyotrophic lateral sclerosis (ALS)
51
What are the three patterns of involvement in motor neuron diseases?
* Mixed UMN & LMN degeneration
* UMN degeneration
* LMN degeneration
52
What type of motor neuron disease is characterized by mixed UMN & LMN degeneration?
Amyotrophic lateral sclerosis (ALS)
53
What is primary lateral sclerosis?
A rare disorder with UMN degeneration, onset after age 50, no LMN signs, and slower progression than ALS
54
What are common symptoms of primary lateral sclerosis?
* Pseudobulbar palsy
* Falling due to balance problems
* Low back and neck pain due to axial muscle weakness
55
True or False: Primary lateral sclerosis usually shortens longevity.
False
56
What are the two types of LMN degeneration?
* Progressive muscular atrophy (PMA)
* Spinal muscular atrophy (SMA)
57
What is Amyotrophic lateral sclerosis?
A degeneration of anterior horn cells and corticospinal tracts in the cervical spine and medulla of unknown etiology
## Footnote
It is characterized by the loss of motor neurons leading to muscle weakness.
58
What type of motor neuron disease is Amyotrophic lateral sclerosis?
A mixed upper and lower motor neuron disease
## Footnote
Upper motor neuron (UMN) involvement leads to mild spasticity in lower extremities (LEs), and lower motor neuron (LMN) involvement causes atrophy and fasciculations in upper extremities (UEs).
59
What are some clinical features of Amyotrophic lateral sclerosis?
Progressive muscle wasting, weakness, and fasciculations
## Footnote
These symptoms worsen over time as the disease progresses.
60
Does Amyotrophic lateral sclerosis involve cognitive dysfunction?
No cognitive dysfunction
## Footnote
Patients typically retain cognitive function despite motor impairment.
61
Does Amyotrophic lateral sclerosis affect sensory or autonomic functions?
No sensory nor autonomic dysfunction
## Footnote
The disease primarily affects motor control without impacting sensory perception or autonomic regulation.
62
What are the initial symptoms of ALS?
Weakness and atrophy of the hands
## Footnote
These symptoms indicate lower motor neuron involvement.
63
What type of neuron involvement presents with spasticity and hyperreflexia of the lower extremities?
Upper motor neuron
## Footnote
This indicates an upper motor neuron lesion.
64
What is the relationship between lower motor neuron symptoms and upper motor neuron symptoms in ALS?
Weakness and atrophy of the hands (lower motor neuron) with spasticity and hyperreflexia of the lower extremities (upper motor neuron)
## Footnote
This demonstrates a mixed presentation of lower and upper motor neuron signs.
65
What are the three main symptoms of the Miller-Fisher variant of GBS?
Ataxia, areflexia, and ophthalmoplegia
## Footnote
This variant may also present with ptosis.
66
What percentage of GBS cases does the Miller-Fisher variant represent?
5% of cases
## Footnote
This highlights the rarity of the Miller-Fisher variant within the broader spectrum of GBS.
67
What serum marker is associated with the Miller-Fisher variant of GBS?
Anti-GQ1b antibodies
68
What is neurosarcoidosis?
Neurologic involvement of sarcoidosis (a systemic granulomatous disease)
## Footnote
Neurosarcoidosis can affect the nervous system, leading to various symptoms and complications.
69
What are the potential effects of neurosarcoidosis on cranial nerves?
May produce multiple cranial nerve palsies
## Footnote
This can lead to a variety of neurological symptoms depending on which cranial nerves are affected.
70
What is the most common neurologic manifestation of neurosarcoidosis?
Diabetes insipidus
## Footnote
This condition is characterized by excessive thirst and urination due to a deficiency in the secretion of the antidiuretic hormone.
71
What treatments can improve symptoms of neurosarcoidosis?
Immunosuppressants (including corticosteroids)
## Footnote
These treatments can help alleviate both systemic and neurologic symptoms associated with the disease.
72
What does PRES stand for?
Posterior reversible encephalopathy syndrome
## Footnote
PRES is also known as reversible posterior leukoencephalopathy syndrome (RPLS)
73
What is the characteristic pattern seen in PRES on imaging?
Widespread vasogenic brain edema
## Footnote
This pattern is typically observed on CT or MRI scans
74
In which regions of the brain is PRES most commonly seen?
Parietal and occipital regions
## Footnote
The most common pattern of PRES involves watershed zones
75
What are the common symptoms of PRES?
* Headache
* Seizures
* Mental status changes
* Focal neurologic deficit
## Footnote
These symptoms can vary in presentation among patients
76
What percentage of patients with PRES may experience intracerebral hemorrhage (ICH) or subarachnoid hemorrhage (SAH)?
Up to 15%
## Footnote
This indicates a significant risk associated with PRES
77
What is the most common pattern of PRES?
Involvement of watershed zones with varying extent in cortex, subcortical and deep white matter
## Footnote
This pattern can lead to a small number of patients progressing to infarction
78
True or False: PRES is always irreversible.
False
## Footnote
PRES is characterized as reversible, which is indicated by its name
79
What types of brain tissue are involved in the PRES pattern?
* Cortex
* Subcortical white matter
* Deep white matter
## Footnote
Involvement can vary among patients
80
What is Giant Cell Arteritis (GCA) formerly referred to as?
Temporal arteritis
81
What type of condition is Giant Cell Arteritis?
Chronic vasculitis of large- and medium-caliber vessels
82
Which arteries are primarily involved in Giant Cell Arteritis?
Cranial branches of the arteries arising from the aortic arch
83
What is the typical age demographic affected by Giant Cell Arteritis?
Age > 50 years
84
Which gender is more affected by Giant Cell Arteritis?
Women, twice as often as men
85
What are some important possible late complications of Giant Cell Arteritis?
* Blindness
* Stroke
* Thoracic aortic aneurysms
* Aortic dissections
86
What diagnostic procedure is recommended for all patients suspected of GCA?
Temporal artery biopsy
87
What is the drug of choice for the treatment of Giant Cell Arteritis?
Corticosteroids
88
Hoe uit polymyalgia rheumatica (PMR) zich?
A condition characterized by muscle pain and stiffness, particularly in the shoulders and hips.
89
How are PMR and giant cell arteritis (GCA) related?
They may be different points on a continuum of the same disease.
90
What genetic marker is frequently associated with PMR and GCA?
HLA-DR4
91
What type of immune response is noted in PMR?
Systemic monocyte activation
92
What percentage of patients with PMR eventually develop GCA?
15%
93
Other name for granulomatosis with polyangiitis
Wegener's disease
94
Other name for eosinophilic granulomatosis with polyangiitis
Churg-Strauss syndrome
95
96
What is Behçet’s syndrome?
A condition characterized by relapsing ocular lesions and recurrent oral and genital ulcers, with occasional skin lesions, thrombophlebitis, and arthritis.
97
What are the main symptoms of Behçet’s syndrome?
* Relapsing ocular lesions
* Recurrent oral ulcers
* Recurrent genital ulcers
* Occasional skin lesions
* Thrombophlebitis
* Arthritis
98
True or False: Behçet’s syndrome only affects the skin.
False
99
Fill in the blank: Behçet’s syndrome includes _______ lesions.
[ocular]
100
Which type of ulcers are associated with Behçet’s syndrome?
* Oral ulcers
* Genital ulcers
101
102
What is fibromuscular dysplasia?
A vasculopathy affecting primarily branches of the aorta
103
What is the most common site of involvement in fibromuscular dysplasia?
Renal artery involvement in 85% of cases
104
What percentage of fibromuscular dysplasia cases are associated with hypertension?
Commonly associated with hypertension
105
What is the incidence of fibromuscular dysplasia?
Approximately 1%
106
What are the characteristic features of fibromuscular dysplasia?
Multifocal arterial constrictions and intervening regions of aneurysmal dilatation
107
What is the second most commonly involved site in fibromuscular dysplasia?
Cervical internal carotid, primarily near C1–2
108
What percentage of carotid angiograms show fibromuscular dysplasia?
1%
109
What is fibromuscular dysplasia's rank among causes of extracranial carotid stenosis?
Second most common cause
110
What percentage of cases have bilateral cervical ICA involvement?
Approximately 80%
111
What percentage of patients with carotid fibromuscular dysplasia also have renal fibromuscular dysplasia?
50%
112
What increased risks do patients with fibromuscular dysplasia face?
Increased risk of intracranial aneurysms and neoplasms, and higher risk of carotid dissection
113
What is the reported incidence range of aneurysms associated with fibromuscular dysplasia?
20–50%
114
What does CADASIL stand for?
Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy
115
What is the inheritance pattern of CADASIL?
Autosomal dominant inheritance
116
Name some clinical features associated with CADASIL
* Migraines
* Dementia
* TIAs (Transient Ischemic Attacks)
* Psychiatric disturbances
117
What abnormalities are typically observed in MRI scans of CADASIL patients?
White matter abnormalities
118
True or False: Anticoagulants are commonly recommended for CADASIL treatment.
False
119
Fill in the blank: CADASIL is associated with _______ disturbances.
psychiatric
120
What type of neurological events are TIAs?
Transient Ischemic Attacks
121
What is pan-cerebellar degeneration?
A type of degeneration affecting the entire cerebellum
## Footnote
It is characterized by the loss of neurons, particularly affecting motor coordination.
122
What is a significant feature of pan-cerebellar degeneration?
Severe Purkinje cell loss due to anti-Purkinje antibodies
## Footnote
Purkinje cells are crucial for motor control and coordination.
123
Mellanby effect
The severity of intoxication is greater at any given level when blood alcohol levels are rising than when falling.
124
What is Wernicke’s encephalopathy (WE)?
A medical emergency characterized by a classic triad of symptoms.
125
What are the components of the classic triad of Wernicke’s encephalopathy?
* Encephalopathy (global confusion)
* Ophthalmoplegia
* Ataxia
## Footnote
All three symptoms are present in only 10–33% of cases.
126
What oculomotor abnormalities are associated with Wernicke’s encephalopathy?
* Nystagmus (horizontal > vertical)
* Lateral rectus palsy
* Conjugate-gaze palsies
## Footnote
Oculomotor abnormalities occur in 96% of cases.
127
What percentage of patients with Wernicke’s encephalopathy experience gait ataxia?
87%
## Footnote
Gait ataxia results from a combination of polyneuropathy, cerebellar dysfunction, and vestibular impairment.
128
What systemic symptoms may accompany Wernicke’s encephalopathy?
* Vomiting
* Fever
129
What is the recommended initial treatment for suspected Wernicke’s encephalopathy?
100 mg thiamine given IM or IV daily for 5 days.
130
Why should thiamine be administered before IV glucose in patients suspected of having Wernicke’s encephalopathy?
IV glucose can precipitate acute WE in thiamine deficient patients.
131
How quickly can thiamine administration improve eye findings in Wernicke’s encephalopathy?
Within hours to days.
132
What improvements can be expected from thiamine administration in Wernicke’s encephalopathy?
* Eye findings improve in hours to days
* Ataxia and confusion improve in days to weeks.
133
What percentage of patients who survive Wernicke’s encephalopathy may develop Korsakoff’s syndrome?
80%
## Footnote
Korsakoff’s syndrome involves disabling memory disturbances, including retrograde and anterograde amnesia.
134
Fill in the blank: Wernicke’s encephalopathy is a medical _______.
emergency.
135
True or False: All three symptoms of the classic triad of Wernicke’s encephalopathy are commonly observed in most patients.
False.
