Week 39- Focal Brain Dysfunction: Seizure Flashcards
1
Q
What is consciousness?
A
A state of awareness of one’s self, place and environment
2
Q
What is the general functions of the cerebrum? (3)
A
- Conscious thought processes –> intellectual functions
- Memory storage and processing
- Conscious and subconscious regulation of skeletal muscle contraction
3
Q
What is the general functions of the cerebellum?
A
Posture, balance, coordination
Complex somatic motor patterns
4
Q
Where is the diencephalon located?
A
Top of the brain stem
5
Q
What are the key components of the diencephalon?
A
Thalamus
Hypothalamus
6
Q
What is the general role of the thalamus?
A
Relay and processing centres for sensory information
7
Q
What is the general role of the hypothalamus?
A
Centres controlling emotion
autonomic functions
hormone production
8
Q
Where is the mesencephalon located?
A
Between the pons and the diencephalon
9
Q
What is the general role of the mesencephalon?
A
Processing of visual and auditory data
Generation of reflex
Maintenance of consciousness
10
Q
Where is the pons located?
A
Bulge in the brainstem –> above the medula oblonggata
11
Q
What is the general role of the pons?
A
Relays sensory information to the cerebellum and thalamus
Subconscious somatic and visceral motor centres
12
Q
Where is the medula oblongata located?
A
Bottom of the brain stem
13
Q
What is the general role of the medula?
A
Relays sensory information to rest of brain stem
Autonomic centres for regulation of visceral function (cardiovascular, resp, GIT)
14
Q
What are Reticular formation in the brain?
A
Embedded in the brainstem –> major nuclear groups for noradrenergic, adrenergic, dopaminergic and serotonergic neurons of the brain
15
Q
What are the two divisions of the Reticular formations in the brain?
A
Lateral reticular formation (parvocellular)
Medial reticular formations (magnocellular)
16
Q
What is the main functions of the Lateral reticular formation (parvocellular)?
A
Reflex connections to local cranial nerve motor nuclei
17
Q
What is the main functions of the Medial reticular formation (parvocellular)?
A
Long ascending and descending axons involved in control of movement, posture, pain, autonomic function and arousal
18
Q
Why do seizures occur?
A
Too much excitatory effects
And/or impaired inhibition
19
Q
What is the roles of the Noradrenergic locus coeruleus?
A
Within the spinal cord –> modulation of autonomic reflexes and pain
Within the cerebrum –> vigilance and responsiveness to unexpected environmental stimuli –> mood regulation
20
Q
What route does the Noradrenergic locus coeruleus take through the brain?
A
Originates in coeruleus locus –> On the superior posterior side of the brain stem to the pons:
Down –> brainstem to spin and cerebellum
Up –> loops to thalamus and hypothalamus and travels around a loop around the corpus callosum.
21
Q
What is the roles of the Dopaminergic cell groups?
A
Influence motor responses by projections to BG (nigrostriatal pathway)
Influence emotion, thought and memory (mesocortical, mesolimbic pathway)
Influence sympathetic preganglionic neurons
22
Q
What are the routes of the Dopaminergic cell groups in the brain?
A
Origin –> ventral tegmental region –> central to triatum under corpus callosum
Origin –> ventral tegmental region –> anterior along frontal lobe
23
Q
What is another name for the serotonergic cell groups?
A
Raphe Nuclei
24
Q
Where are Raphe nuclei (serotonergic cell groups) located?
A
Medial line up the brainstem
25
What is the roles of the serotonergic cell groups?
1. Motor and autonomic system of spinal cord
2. Modulate pain
3. Hypothalamic cardiovascular and thermoregulatory control
4. Forebrain responsiveness of cortical neurons and regulation of sleep-wake cycles and mood
26
What is the route of the serotonergic neuronal circuits in the brain?
Loops everywhere:
Stem --> cerebellum
Stem --> basal ganglia and corpus callosum
Stem --> loop anterior via frontal all the way to occipital
27
What is the roles of the neuronal circuits with Cholinergic Cell groups?
PMT (pontomesencephalo-tegmental complex) and basal nuclei -->influences cortical arousal during waking states and dreaming (REM)
Medial septal nuclei --> hippocampus, memory and learning
28
What is the route of the Collinergic Cell groups?
Brain stem nears pons loops around frontal to occipital
29
What is the role of the Histaminergic cell group?
Help maintain arousal in forebrain (explains drowsiness caused by antihistamines crossing the BBB)
Arousal response
30
What are some examples of the monoaminergic cell groups?
Noradrenaline, serotonin
31
What are the effects of the noradrenaline and serotonin cell groups within the cerebral cortex and thalamus?
Wakefulness and responsiveness of cortical and thalamic neurons to sensory stimuli = arousal
32
What are the two major cholinergic pathways?
Inputs from pedunculopontine and laterodorsal tegmental nuclei:
1. To intralaminar nuclei of thalamus --> projecting widely upon the cortex
2. Lateral hypothalamic area to join with hypothalamic and basal forebrain cholinergic projections to cortex
33
Where is the central sulcus located and what direction does it run?
Midbrain --> coronal
34
What two areas does the central sulcus separate?
```
Primary Motor cortex (front)
Somatosensory cortex (back
```
35
What is the role of the primary motor complex?
Voluntary movement
36
What is the role of the somatosensory cortex?
Somaesthetic sensation and proprioception
37
What lies anterior to the primary motor complex?
Premotor complex
38
What is the role of the premotor complex?
Coordination of complex movements
39
What is anterior to the premotor complex?
Frontal lobe
40
What is the role of the frontal lobe?
Planning of voluntary activities
Decision making
Personality traits
41
What is the small area within the inner brain posterior to the frontal lobe?
Broca's area
42
What is the role of Broca's area?
Speech formation
43
What is the two main lobes on the lateral sides of the brain?
Temporal lobes
44
What is the role of the temporal lobes?
Integration of sensory inputs
45
Where is the primary auditory complex located?
Middle superior edge of the temporal lobes
46
Where is the limbic association cortex located?
Mostly inner and bottom surface of temporal lobe
47
What is the role of the limbic association cortex?
Motivation
Emotion
Memory
48
Where is the occipital lobe located?
Posterior side of brain (above cerebellum)
49
Where is the primary visual cortex?
Posterior edge of occipital lobe
50
What is the lobe behind the somatosensory cortex?
Parietal lobe
51
What is the roll and location of the posterior parietal cortex?
Integration of somatosensory and visual input --> important for complex movements
Located --> immediately posterior to somatosensory cortex
52
Where is Wernicke's area located?
Inner of the parietal lobe (posterior brain)
53
What is the role of Wernicke's area?
Speech understanding
54
Where is the PFC orbitofrontal?
Inferior side of the frontal cortex (as it wraps back under the brain and tucks in near the temporal lobes)
55
What are deficits in the PFC orbitofrontal linked with?
```
Disinhibition
Altered personality
Lack of empathy
Socially inappropriate behaviour
Reactive aggression
```
56
Where is the dl-PFC (dorsolateral)?
Lateral side of the prefrontal cortex both sides)
57
What are some affects of deficits in the dl-PFC?
Reduced attentional control
Preseveration
Impaired exacutive functions (working memory, sequencing, planning, creativity, reasoning)
58
Where is the medial prefrontal cortex (m-PFC)?
Medial inner wrap around of the frontal lobe (sits under the corpus callosum frontal protrusion)
59
What are deficiets in the m-PFC linked to?
Decreased motivation
Apathy
Akinesia
Impaired detection of mismatches or errors
60
What does arousal and wakefulness depend on?
Functioning of the cerebral hemispheres and the reticular activating system of the brainstem
61
What does content and cognition; emotions (affect) depend on?
Functioning cerebral cortex
62
What is unconsciousness?
Lack of such awareness/responsiveness
63
What is the general states which are regarded as conscious?
```
Being awake from low levels to high levels of alertness:
Drowsiness
Indifference
Normal quiet state
Vigilance
Hyper-arousal
```
64
What are some levels low to high in terms of unconsciousness?
Sleep
General anaesthesia
Coma
Vegetative state
65
What is the clinical aspects of confusion?
Issues with self, space and time
66
What is clinical delirium?
Reduced awareness of the environment
Reduced attention
Changes in cognition (false beliefs)
Changes in perception (hallucinations)
67
What is clinical obtundation?
Mental blunting with mild to moderate reduction in alertness
Reduced pain sensation
Can happen in trauma, mistreatment or psychological stress
68
What is clinical Stupor?
A state of lethargy and immobility with diminished responsiveness to stimulation
69
What are the 5 wave types seen on an ECG?
```
Delta
Theta
Alpha
Beta
Gamma
```
70
What is the Hz and situation were you would see Delta EEG activity?
< 4 Hz --> slow-wave sleep/ coma
71
What is the Hz and situation were you would see Theta EEG activity?
4-7Hz --> drowsiness
72
What is the Hz and situation were you would see Alpha EEG activity?
8-15 Hz --> relaxed wakefulness
73
What is the Hz and situation were you would see Beta EEG activity?
16-30 Hz --> active wakefulness
74
What is the Hz and situation were you would see Gamma EEG activity?
30-100 Hz --> mainly a artifact introduced by muscular activity
75
What are the origins of EEG readings?
Synchronous contribution from a very large number of neurons
76
What potentials contribute to EEG waves?
Post synaptic potentials (excitatory and inhibitory)
| Aps
77
What picks up the EEG reading?
EEG electrode on the outside of the skull
78
What is resting membrane mainly determined by?
Mainly by the concentration gradient of K+ --> loss of K+ results in the negative charge seen in neurons.
79
Where is K+ and Na+ in higher concentration in regards to cells?
K+ higher inside cells
| Na+ higher outside the cells
80
What allows for the generation of transmembrane potentials and ion concentration gradients across cell membranes?
Na+/K+ ATPase
81
What is an Action potential?
Nerve impulse --> electrical spike which can propagate along the axon
82
What triggers neurotransmitter release at the presynaptic region?
Opening of voltage gated Ca+ channels triggers vesicle mobilisation and release
83
What is depolarisation?
Change in voltage driving the resting potential towards 0 from the resting negative voltage
84
What is hyperpolarisation?
Increase in the negative potential --> further polarised
85
What is the three main phases of action potentials?
Depolarisation
Repolarisation
Undershoot (hyperpolarisation) --> relative refractory period
86
How do ions flow in voltage gated ion channels?
According to pre-existing electrochemical gradients (after required voltage is achieved)
87
What is some typical domains of Na voltage gated channels?
S4
| S5-S6
88
What is the mechanism of S4 domain voltage channel gates?
S4 --> voltage sensor --> sensor is positively charged --> when voltage changes it undergoes a conformational change --> gating
89
What is the mechanism of S5-S6 domain voltage channel gates?
S5-S6 --> pore loop domains
90
What is the two subunits within voltage gated sodium channels?
Single Na alpha subunit forms complex with auxillary Na Beta subunits
91
What is the activation gate for voltage gates channels?
Gate that opens inside the cell membrane to open the channel
92
What is an inactivation gate?
Time dependant gate present in Na channels
93
What is a way apart from voltage is voltage gated Na channels regulated?
Phosphorylation
94
What is the impact of phosphorylation on voltage gated sodium channels?
Can slow its inactivation
95
What gate is responsible for the rising phase in action potential?
Voltage gated sodium channels opening
96
What makes the voltage gated sodium channels to stop functioning and allow for repolarisation during an action potential?
Time dependant inactivation gates
97
How does tetrodotoxin have its affect?
Prevent Na+ flow by binding to the outside of the pore
98
What is the structure of a voltage dependant calcium channel?
Single alpha subunit forms complex with axillary subunits (similar to Na+)
99
How are Ca+ voltage dependant calcium channels subtyped?
According to their alpha subunit and their threshold of activation (low or high voltage activated)
100
What do calcium voltage channels normally respond to?
Membrane depolarisation
101
What is the structure of the voltage dependant potassium channel?
Four alpha subunits each containing 6 subunits (S1-S6) and a membrane re-entering P-loop
102
What phase are K+ voltage channels involved in?
Repolarisation phase (efflux of K+ repolarises cell)
103
What is the structure of a voltage gated chloride?
Subunits contain multiple transmembrane domains and channels arranged as dimers (each subunit contains a pore)
104
What determines the speed of a voltage gated chlorine channel?
The opening and closing of the dimer pores.
Fast gating --> when pores are individually opened and chlorine can pass with just 1 open
Slow gating --> when both pores need to be open before chlorine can pass
105
What makes ligand gated ion channels open?
Typically requires binding of one or more neurotransmitter molecule
106
What are some examples of excitatory ligand gated ion channels?
Nicotinic
NMDA
AMPA
107
What is an example of a inhibitory ligand gated ion channel?
GABA
108
What type of proteins are the nicotinic acetylcholine receptors?
Ligand gated Na+ enters/K+ exits channel
109
What is the effect of the Nicotinic acetylcholine receptors?
Movement of cations --> excitatory response in post synaptic cell
110
What activates the NMDA receptor?
Glutamate
111
What movement does NMDA receptor allow?
Influx --> Sodium and calcium
| Efflux --> Potassium ions
112
What activates the AMPA receptor?
Glutamate
113
What ions are moved through the channel activated by the AMPA receptor?
Influx --> Na+
| Efflux --> Potassium
114
Are NMDA and AMPA excitatory or inhibitory?
Excitatory
115
Is GABA-A receptor excitatory or inhibitory?
Inhibitory
116
What channels do GABA A receptors activate?
Chloride ion channels
117
What types of receptors control depolarisation?
Sodium
Calcium
AMPA and NMDA
118
What types of receptors control polarisation/hyperpolarisation?
Potassium
| GABA-A
119
What is the most common ion channel type at the presynaptic side?
Voltage gated
120
What is the most common ion channel type at the post-synaptic side?
Ligand gated
121
What happens to cortical neurons during seizure?
Abnormal, hypersynchronous discharge of a population of neurons
122
What is Epilepsy?
Group of neurological disorders which exhibit recurrent seizures unprovoked by acute systemic or neurologic insult
123
What happens during seizure initiation?
Sudden membrane depolarisation for a few seconds
Burst of action potentials
Abnormal and excessive synchronisation of neighbouring populations of cortical cells
Triggered by --> missed meds, drugs/alcohol, lack of sleep, hormones, stress, lights, noise
124
What is the accompanied burst of action potentials in seizures known as?
Paroxysmal depolarising shift
125
What happens during seizure propagation?
Partial seizure spreads within the brain
126
What are the steps of seizure propagation?
Activation of nearby neurons (abnormally activated) --> prolonged action of excitatory transmitter
Loss of surrounding inhibition --> loss of brakes
127
How can hyperexcitable states arise?
Too much excitation --> sustained overt depolarisation
| Too little inhibition --> defects in hyperpolarisation --> low GABA etc
128
What does repetitive discharge lead to?
Accumulation of Ca2+ in presynaptic terminals --> enhances neurotransmitter release
Depolarisation induced NMDA activation --> enhances neurotransmitter release
Increase in extracellular K+
129
What kind of mutations have been identified in epilepsy?
Ion channel mutations of both:
Excitatory channels --> that switches it on
Inhibitory channels --> that switches it off
130
What do many epileptic drugs target?
Voltage gated and ligand gated ion channels
131
What is the paroxysmal depolarisation shift?
Prolonged depolarisation with rapid spikes in a synchronous way
132
What is surround inhibition within neuronal activity?
The areas surrounding a central signal are inhibited to sharpen the contrast between the signal
133
What does surround inhibition normally prevent?
Synchronisation of adjacent neurons
134
What is the goals of treatment with anti-epileptic drugs?
Suppress existing seizures and also decrease probability of future seizures
135
What are the three activation states of voltage-gated sodium channels?
```
Resting state (closed)
Activated state (open)
Inactivated state (closed)
```
136
Do phenytoin, carbamazepine and Lamotrigine all bind to the same spot on the voltage gated sodium channel?
No --> different areas
137
What is the mechanism of Phenytoin and Carbamazepine and Lamotrigine?
Decreases rate of recovery of voltage-gated Na+
channels --> prevents rapid firing of neurons
Phenytoin --> does not affect GABA or Glu transmission
Lamotrigine --> impedes Glu release to prevent excitatory transmission
138
When is Phenytoin indicated for use?
Most seizure types
NOT absence seizures
NOT good for temporal lobe epilepsy
139
What is carbamazepine indicated for?
Used for most seizure types --> unlike phenytoin it is the drug of choice for temporal lobe epilepsy
NOT good for absence seizures
140
When is Lamotrigine indicated for use?
Used for many seizure types INCLUDING absence seizures
141
What is the function of Barbiturates like phenobarbitone?
Augments neuronal inhibition via GABA-A receptors:
Prolongs duration but not the frequency of GABA currents
Limits sustained repetitive firing at higher concentrations
142
What is the mechanism behind barbiturates function?
They are channel modulators --> they act like a chemical "stent" to keep the channel open longer
They are NOT agonists
They just make the channel stay open longer when it does open they do not open the channel
143
What other affects do Barbiturates have apart from their action on GABA channels?
Can inhibit voltage gated Ca2+ channels --> mediates decreased Glu release and thus decrease excitotoxicity neurotransmission
Can have some sedative activity --> tolerance develops rapidly
144
What seizures are Barbiturates indicated?
Tonic-closure, partial seizures, absence seizures
145
What do Benzodiazepines do?
Augment neuronal inhibition via GABA-A receptors --> they increase the frequency in which the Cl- ion channels are open (not the duration)
Drives influx of Cl- --> inhibits activity and stabilises membranes of target neurons
146
Are Benzodiazepines agonists?
Yes
147
What paediatric seizures are benzodiazepines indicated for?
Myoclonic and absence seizures
148
What is an example of a Benzodiazepine?
Clobazam
149
What does clonazepam get used for?
Standing treatment
Status epilepticus
Also inhibits T-type calcium channels which makes it useful for absence seizures
150
What does gabapentin do?
Changes GABA release from neurons
| Inhibits high voltage activated calcium channels --> less neurotransmitter release
151
What seizures is gabapentin used for?
Partial seizures with or without secondary generalisations
| --> often in conjunction with other drugs
152
What neurons does ethosuximide target?
Thalamic neurons only
153
What is the affect of ethosuximide?
Blocks low-threshold Ca2+ channels
Reduces current --> prevent electrical activity spread (hallmark of absence seizures)
No affect on inactivation state, recovery time or voltage dependence of currents
No affect on GABA, Glu or repetitive firing
154
What seizures are ethosuximide (thalamic calcium channel blocker used for)?
Absence seizures
| Cant be used for other seizures --> can trigger tonic-clonic seizures
155
What is valproate indicated for?
All types of seizures including absence seizures
| NOT used for temporal lobe epilepsy
156
How many mechanisms does Valproate have?
3
157
What are the 3 mechanisms of Valproate?
1. Prolongs recovery rate of Na+ channels --> similar to phenytoin and carbamazepine
2. Inhibits T type Ca2+ channels --> in thalamic neurons to treat absence seizures
3. Augments GABA production and impedes metabolic breakdown which changes resting potentials --> reduces chance of AP
158
What is topiramate indicated for?
Partial and generalised tonic-clonic seizures
159
What is the mechanism of topiramate?
Blocks voltage gated Na+ channels
Activates K+ hyperpolarising currents
Enhances post-synaptic GABA-A activity
Limits activation of AMPA and glutamate receptors
160
What is the issue of anti-convulsant and pregnancy?
They are associated with birth defects
161
What is the term for a drug that disturbs development of an embryo/foetus?
Teratogenic
162
How has incidence and types of defects been monitored for anti-convulsant association?
Voluntary registries to track
163
What is the malformation rate during pregnancy with use of anticonvulsants?
6% on average
| But no good data on actual risk
164
What are some types of birth defects associated with anticonvulsants?
Spina bifida
Cleft palate
Congenital heart defects
Microcephaly
165
What is a seizure?
A seizure is a sudden, uncontrolled electrical disturbance in the brain. --> usually of abnormal and excessive synchronisation of a population of cortical neurons
166
What is the mechanism behind seizures?
An increase in excitation or a decrease in inhibition --> affects of ion channel disturbances leads to the synchronisation of groups of neurons with large depolarisations happening at once.
167
What are some common causes of seizures?
```
Abnormal levels of glucose
Abnormal electrolytes (Na+, K+ and Ca2+)
Traumatic brain injury
Stroke
TIA
Fever
Drug abuse
Epilepsy
High blood pressure
Intracranial mass
```
168
What is epilepsy?
Epilepsy is a chronic disorder that causes unprovoked, recurrent seizures.
169
How does epilepsy differ from seizure?
Epilepsy is the increased chance for chronic or reoccurring cases of seizure
Seizure can be termed when it is a chance occurrence and not an ongoing predisposition
170
What are the two main seizure types?
1. Focal /partial seizures
| 2. Generalised seizures
171
What are focal seizures?
Focal seizures are seizures which originate in one area or side of the brain.
172
What are generalised seizures?
Wide spread seizure activity in the left and right hemispheres of the brain
173
What are the two main types of focal seizure?
Focal seizure with retained awareness (simple partial seizure)
Focal seizure with loss of awareness (complex partial seizure)
174
What are the different types of generalised seizures that may occur?
```
Absence seizures
Tonic-clonic
Atonic seizures
Clonic seizures
Tonic seizures
Myoclonic seizures
```
175
What might a focal seizure look like?
Frontal lobe --> motor --> kicking, pedaling, twitching, head or eyes turn
Occipital --> lights, colours, visual change, eyelid fluttering
Parietal lobe --> numb, odd sensation in affected area, struggle reading, writing
Temporal lobe --> auditory halucinations/changes, odd taste/smell
Etc --> normally one sided affects as starts on one side of the brain
176
What are some features of an absence seizure?
Lapses of awareness --> staring for a few seconds
Person is unaware during the seizure normally
Immediate recover after the seizure
177
What does tonic/clonic refer to?
```
Tonic = normal muscle tone
Clinic = rhythmical jerking
```
178
What happens during myoclonic seizures?
Quick uncontrolled muscle jerks
179
How can an EEG change in response to a seizure?
There will be a large increase in activity
Focal --> in focal seizures only a few leads will be impacted
Generalised --> lots more leads will show an affect
180
What can be some psychosocial impacts of seizure disorders?
People may be scared, treat you differently
Impacts ability to drive
Requires sustained treatments
181
What are some other space occupying intracranial lesions other than tumours?
Cysts
Parasites
Haematoma
Inflammatory
182
Common causes of headache?
```
Stress
Lack of sleep
Fatigue
Hunger
Withdrawal (caffeine etc)
Alcohol
Some food and drink
```
183
What is myasthenia gravis?
Disorder of neuromuscular junction --> Ach receptor issue --> leads to muscle weakness
184
What is the difference between benign vs malignant?
Benign --> does not invade surrounding tissue
| Malignant --> invades surrounding tissue
185
What is a primary brain mass?
Tumours from cells in the brain
186
How common is primary masses in the brain?
1.2% of all new cancers
187
What is a secondary mass?
Tumours from the cells from outside the brain
188
How common are secondary masses in the brain?
10 times more common than primary brain masses
189
What can be some of the effects of tumours on the brain?
Local brain invasion
Compression
Raised intracranial pressure
190
How are brain metastasis diagnosed?
```
Symptoms of cancer
Evidence of cancer elsewhere
Focal neurological deficits
CT
MRI brain
Biopsy --> hard to get biopsy --> not needed normally
```
191
How do paediatric brain masses differ to adult brain masses?
Paediatric --> primary are second most common cancer --> leading cause of death (20% of childhood malignancies)
Adults --> most in cerebral cortex --> Gliomas, meningiomas, pituitary tumours
192
What are some risk factors for brain tumours?
```
Majority are sporadic but:
Ionising radiation
Hereditary syndromes:
Neurofibromatosis
Von Hippel Lindau
Tuberous sclerosis
```
193
How common are benign vs malignant brain masses in adults?
2/3 benign, 1/3 malignant
194
What is the most common benign tumours in adults?
Meningiomas
195
What cancers is radiation primary treatment?
Prostate, head and neck, cervix, lung, oesophagus, skin bladder, brain, lymphoma
196
Can radiation be used palliatively?
Yes
197
What are the sources of radiation for therapy?
External beam --> linear accelerator, non invasive --> targeted to area
Brachytherapy --> radioactive source (eg Iridium 192) placed next to point of interest
198
What kind of radiation is used for therapy?
X rays
199
Why is the multiple treatments normally for radiation therapy?
Total dose needed to maximise chance of cure --> if does in one go there ill be bad side effects
Normal tissue gets to recover
Make sure the treatment targets cancer cells in the right cell cycle phase
200
What is the standard dose unit for radiation therapy?
Gray (Gy)
| 1 Gy is Joule absorption per Kg
201
How does radiation therapy cause cancer cell death?
DNA damage and induced cell apoptosis/death
202
Where do the side affects of radiation occur?
Locally to the treatment site
203
What does adjuvant mean?
Radiation is an addon treatment
204
What is palliative treatment?
Helps with pain and other symptoms on a short term
205
What are some side affects of radiation therapy?
```
fatigue (tiredness)
dry, red or itchy skin.
loss of appetite.
nausea (feeling sick)
digestive problems.
hair loss.
dry or sore throat or mouth.
cough or shortness of breath.
```
