Confusion (delirium) Flashcards
Define confusion
Confusion = acute, treatable or chronic progressive condition
Patient has the inability to think clearly and / or rapidly characterised by:
- Difficulty understanding a situation
- disordered or unclear thoughts
- associated with memory loss and/or disorientation
Can be aggravated by environmental or diurnal changes e.g. sundowning
How common is confusion?
Who is it more common in?
1/10 hospital patients will be confused at some point
More common in:
Elderly
People w:
memory problems
poor hearing/ eyesight
recent surgery
terminal illess
people with a brain disorder e.g. stroke or tumour
Where do we most often see confused patients?
most commonly:
at home
in residential and nursing homes
in hospital –> post op, A & E, wards
Being in hospital makes confused patients more confused, we try and manage them as much as possible in their home
What are some common causes of confusion?
Infections
Head injury
Stroke
Brain or spinal cord tumour
Dementia
Delirium
Alcohol or drug intoxication
Sleep disorder
Chemical/ electrolyte imbalances
Vitamin deficiencies
Medication
Seizure
Hypothermia
What are the pathways implicated in confusion?
What are the two sites of production of this NT?
Where do these sites of NT production project to?
Therefore what is this NT involved in and how would changing its levels change a pt?
The pw’s involved in confusion are the cholinergic pathways.
Cholinergic:
- Nucleus basilis of meynert, (situated under the nucleus accumbens and related to reward pathways) projects to cortical regions and striatum (supplies cortex and limbic system)
- Brainstem pontine nuclei (involved in control of arousal) –> two nuclei produce Ach in the brainstem:
- Lateral tegmentum (Also produces dopamine)
- pedunculopontine nucleus (involved in arousal)
- Intrinsic cholingeric systems are also found within the striatum and hippocampus –> Hippocampus involved in memory, striatum involved in movement as well as neurocognitive behaviours.
- Changing Cholinergic levels will affect motor system, higher cortical functioning, cognition.
- Brainstem regions project up to thalamus (linked to sleep) and down the spinal cord
- Therefore there is both a central and peripheral effect by medications added to this p/w
What role does ACh play in arousal?
- Peripherally controls ANS and muscle function (NMJ)
- Centrally involved in:
- Alertness
- Arousal
- Attention
- Sleep
- Memory
- Learning
- Acetylcholine also modulates a no of NT pw’s including dopamine.
What are the two transmitters involved in the sleep wake cycle? (part of the arousal spectrum).
Transmitters involved in sleep wake cycle:
Histamine
Acetycholine (Ach)
Describe the waking stage of sleep wake cycle
Waking:
- High levels of histamine which activate cholinergic pathways
- Cholinergic pathways activate the thalamic reticular nuclei
- Enables information to flow freely though this area
- Information flow –> awareness and arousal –> conciousness
Describe the changes that occur during slow wave sleep
- Histamine levels start to drop, less activation of cholingergic pw’s, less cortical activity
- Low light and warmth detected by suprachiasmatic and ventrolateral preoptic nuceli (hypothalamus)
- Inhibits the histamine cells in the tuberomamillary bodies and brainstem
- Inhibits the cholinergic pw/s
- reduced activity passing through the thalamus
- Prevents info flow –> low arousal level
Describe the changes in REM sleep
Paradoxical or REM sleep:
- During deep sleep (slow wave sleep) you have slow delta waves that oscillate, controlled by the thalamus which acts as the gatekeeper of activity.
- The thalamus prevents output to the cortex with its own intrinsic rythm
- In REM sleep, cholinergics are activated again, allowing some cortical activity again (dreaming) and allows movement (eye movements):
- Inhibition increases which begins to affect other NT pw’s
- 5HT and NA (which normally dampen cholingergic activity) decrease
- Increased cholinergic input to the thalamus
- Increased cortical activity (active mind in an inactive body).
What is sundowning syndrome?
What sx may a pt present with?
Best approach?
Sundowning syndrome –> the closer to evening and sundown the more confused and agitated the client becomes (those with dementia feel they should be busy at this time)
Late day confusion
Link between arousal levels and diurnal rhythm
Sx: agitatation and increased movement
Most important thing to do is to find out their normal routine, keep them busy and it will eventually reside.
What contributes to sundowning?
1) Cholinergic abnormalities –> reduced input of Ach from Nucleus basalis of meynert (NBM) to cortex
2) Disrupted sleep patterns –> reduced sleep efficienct, frequent awakenings, daytime napping
3) Reduced zeitgebers (light sent to suprachiasmatic N in hypothalamus to control diurnal rhythm)–> dim daytime light, disruptive light at night, lack of daily routine
4) reduced physical activity
5) reduced melatonin –> decreased production, reduced receptor sensitivity
6) SCN (suprachiasmatic nucleus) degeneration –> loss of cell, loss of diurnal rhythm, AVP and VIP
What can you suggest to reduce sundowning syndrome?
- Routine
- reduce light interferences
- regular wake-sleep cycles
- Regular eating patterns
- Exercise / activity
- reduce stress
Describe the link between DA and Ach?
- ACh can modulate activity in dopamine pathways (and vice versa) –> nigrostriatal (movement), mesocortical and mesolimbic pathways (cognition, emotion, reward pathways), tuberohypophyseal
- This will also have knock on effects on other monamines: NA and 5HT –> changes arousal levels as involved in keeping you awake/ alert
- ACh neurons in striatum modulate PFC and are abundant in the hippocampus
- Striatum releases Ach which affects the cortical input before its fed into the motor system
- Affects pw’s from prefrontal cortex (higher cog) and to the limbic system
- Affects input from the midbrain, where most of the DA pw’s come from (VTA and substantia nigra).
What is the reward pw?
How can Ach control the reward pw?
- Reward pw= mesocortical pw –> involves DA from the VTA –> nucleus accumbens –> prefrontal cortex, positive emotional pw
- Ach acts at all levels of the reward pathway:
- Nucleus basilis of meynert (NBM) acts on the nucleus accumbens
- Ach also produced in the brainstem ( pontine centres) and therefore can act on the ventral tegmental area
- Therefore Ach affects how DA reaches the midbrain and how it reaches the cortex.
- NBM and local interneurons act within the prefrontal cortex
How can Ach control motor activity?
Ach acts to alter activity in the striatum via interaction with GABAergic pathway
It does the exact opposite of dopamine:
–> dopamine normally activates the direct pw
–> Ach inhibits the direct pw (Reduces movement)
–> Dopamine normally activates the indirect pw
–> Ach inhibits the indirect pw
Degeneration of cholingeric interneurons can lead to increased or decreased motor activity and changes in motivation
How does Ach relate to confusion?
Reduced levels of Ach lead to imbalance in limbic system, prefrontal cortex, basal ganglia and brainstem
This leads to:
- Slower reduced recall, memory
- Changes in decision making
- Altered motor function
- Altered arousal states and orientation
What is delerium?
Delirium = Acute confusional state
Medical emergency, usually transient, reversible but it CAN have a poor outcome.
Develops over a couple of days
What is delerium characterised by?
What can it often be misdiagnosed as?
- Decreased attention span
- Waxing and waning confusion
- Plus a wide range of other neuropsychiatric abnormalities
Often misdiagnosed as dementia, depression, schizophrenia, mania or normal ageing.
What are the types of delerium?
Three types of delerium:
1) Hyperactive –> pts have heightened arousal, can be restless, agitated, aggressive
2) Hypoactive –> pts become withdrawn, quiet, sleepy
3) Mixed –> combination of hyper and hypoactive
What are the characteristics of hyperactive delerium?
- Confusion
- Pereceptual changes –> auditory, visual hallucinations
- Sleep disturbance
- Agitation
- Restlessness
- Lack of cooperation
- Changes in communication
- Mood/ attitude changes
What are the key indicators of hypoactive delerium?
- Worsening concentration
- Slowness of responses
- Reduced movement and or mobility
- Appetite changes
- Reduced social interaction/ withdrawal
What are the risk factors for delerium?
- If any of these risk factors are present person is at risk of delerium:
- Age > 65 years
- Cognitive impairment (past or present) and/ or dementia
- Current hip fracture (35% - 61%)
- Severe illness (deteriorating or at risk of deterioration)
- Observe people at every opportunity for any changes in the risk factors for delerium.
What are come of the main causes of delerium?
Remember Mnemonic (then try to remember each class)
TEN DIMES
Trauma –> Head injury
Epilepsy –> post ictal
Neoplasia –> primary cerebral malignancy, secondaries in brain, paraneoplastic syndromes
Drugs –> prescribed drugs (benzoD, Analgesics (morphine), Anticholinergics, anticonvulsants, antiparkinsonism, steroids
Infection –> UTI, Pneumonia, sepsis, meningitis/encephalitis/cerebral abscess, malaria, viral
Metabolic –> Hypoxia, electrolyte abnormalities (hyponatraemia, hypercalcaemia, hypo/hyperglycaemia, hepatic and renal impairment, Vitamin deficiencies –> Thiamine, nicotinic acid, vitamin B12
Endocrinopathies –> hypo/hyperthyroidism or parathyroidism, hypopituitarism, cushing’s, porphyria, carcinoid
Substances (toxic) –> Alcohol (acute intoxication or withdrawal), CO poisoning, exposure to heavy metals, barbiturate withdrawal
What are the reversible causes of delerium?
Reversible causes of delerium include:
Drugs
Emotion (mania or agitated depression)
Low oxygen (ischaemia, congestive heart failure, stroke or pulmonary embolus)
Infection
Retention (urine or faeces)
Ictal states
Undernutrition
Metabolic (thyroid function or organ failure)
What are the reversible causes of dementia (of alzheimer’s type)?
Drugs
Emotional illness (incl. depression/ schizophrenia
Metabolic/ endocrine disorders
Eye/ear/environment
Nutritional/ neurologic
Trauma
Infections
Alcoholism/ anaemia/ atherosclerosis
What are the common features of delerium (opposed to dementia)
Mode of onset –> acute/ subacute
Poor attention –> characteristic
Concsious level –> often affected –> may be wild fluctations
hallucinations/ misinterpretations –> common
fear, agitation, aggression –> common
Exteremely disorganised thought patterns w unrealistic ideas –> common, often flights of fancy
Motor signs –> myoclonus, postural tremor, flapping tremor (asterixis)
speech –> slurred
dysphasia –> none
Dyspgraphia –> often prominent
short and long term memory –> poor
What are some of the common features of dementia (opposed to delerium)?
Mode of onset –> chronic, subacute
poor attention –> later event
Consious level –> normal
Hallucinations and misinterpretations –> late events
fear, agitation, aggression –> not common in early stages
Extremeley disorganised thought patterns w unrealistic ideas –> late feature (poverty of thought)
Motor signs –> none or late feature
speech –> normal
dysphasia –> often present
dysgraphia -> if present in keeping w degree of dementia
short/ long term memory –> often normal until late
Describe the pathphysiology of delerium vs dementia
- Amount of neural cell death and neuroinflammatory response determines development of delerium vs dementia
- levels and duration of inflammation and response to this determines outcome
- Inflammatory mediators cross the BBB
- Causes activation of the microglia
- Triggers neuroinflammation
- Dysfunction or death will ensue:
- neuronal dysfunction –> delerium of short or long duration
- Short duration can return pt to normal
- Long duration –> pt will have some abnormality
- neuronal death –> dementia
- neuronal dysfunction –> delerium of short or long duration
What are the neurotransmitters involved in delerium?
What area of the brain will be massively affected?
Inflammation of tissue leads to:
Decreased cholinergic activity –> which has a knock on effect on the dopamine system
Increased dopamine activity
Increased serotonin activity –> boots up autonomic activity, increased HR, increased agitation levels
Decreased GABAergic transmission (cholingeric pw interacts massively with GABA)
Increased stress hormones
Key area that will be affected by cortisol –> amygdala (fear and hallucination).
What are the causes of hallucinations?
Delerium
Dementia
Psychiatric disorders –> schizophrenia, psychosis
Drugs (lsd), alcohol, medications
Epilepsy – >focal seizures
Narcolepsy
Visual impairment –> charles bonnet syndrome
Hallucinations can be normal :
–> part of grief process
–> hypnagogic (falling asleep) and hypnopompic (waking) hallucinations
Describe fMRI cerebral activity during a hallucination
Hallucination –> spontaneous activation of sensory centres as if you were actually percieving it, fMRI shows the activity within the visual areas/ perceptual areas
Shows activity as if the hallucination is real
Hallucinatory acitivity overrides actual sensory inpt
Thought there is a temporary disconnect between the cortical and thalamic regions (not allowing real sensory info through the thalamus to the cortex).
What are the circuits involved in psychosis?
Dopaminergic pathways
Prefrontal cortex –> dorsolateral and ventrolateral linking to the limbic systerm
Anterior cingulate gyrus
Basal ganglia –> striatum
Hippocampus
Cerebellum –> pattern of speech and thought are changed, become repetitive and rhythmic
Describe the limbic system
What structures are included?
Limbic system = group of deep cortical and subcortical structure which includes:
Hippocampus
Amygdala
Nucleus accumbens (reward pw)
Cingulate gyrus –> reasoning pws cognitive function
Mamillary body
Thalamic and hypothalamic nuclei
Entorhinal and perirhinal cortices
Links to Insula (hidden lobe) moderates emotional responses and links limbic to homeostatic regions, also contains taste centre
What are the 4 key functions of the limbic sx?
Memory
Learning
Perception (sensory, emotional, spatial)
Motivation
What region of the cortex does the limbic sx particularly link to?
What is aided by the integration of this info to this region?
Interplay w/in limbic sx and particularly the pre frontal cortex aids integration.
Integration of info relevant to:
Arousal
Learning
Memory
Emotion
Higher cognition
Describe the pathways involved in reward and fear and what areas modulate our response
Regions of the limbic sx are implicated in both positive and negative emotions
Nucleus accumbens linked to reward wherase amygdala linked to negative emotion
The uncinate fascicuus links the amygdala to the PFC
the Insula sets the threshold of the response
Hippocampus puts everything into context and remebers it
What does the Prefrontal cortex refer to?
Pre frontal cortex refers to any region of the frontal lobe preceding the motor areas
Main roles: integration and decision making
Responsible for personality
Label image
What is the prefrontal cortex involved in?
1) Restraint behaviours:
concentration
judgement
foresight
focus
2) initating behaviours
motivation/ drive
spontaneity
personality
curiosity
3) ordering behaviour
Planning/ sequencing
Working memory
Abstract thought
Perspective
What connects the PFC and the limbic system?
What is the role of this connection?
What other regions does the PFC connect to?
What sets emotional thresholds?
What is a change in activity in these circuits related to?
Massive connections between the PFC and limbic sx is the uncinate fasciculus. It connects the PFC to the uncus.
(Uncus is the anterior most part of the parahippocampal gyrus, part of the olfactory cortex)
Massive interconnection between PFC and primary sensory areas.
Insula sets emotional thresholds
Any change in tract activity detected in confusion, psychotic episodes, major depressive disorders and bipolar disorders.
Name the fibre tract that connects the prefrontal cortex to the medial temporal lobe
Why does raised ICP lead to personality changes?
The uncinate fasciculus
Raised ICP can lead to uncal herniation which can compress the uncinate fasciculus, changing the interplay between the PFC and limbic system.
What are the 3 main attentional circuits?
- Default mode network
- Medial temporal cortex
- medial prefrontal cortex
- posterior cingulate gyrus
- tells you where you are
- Dorsal attentional network (oreinting and processing)
- Dorsolateral prefrontal cortex
- Posterior parietal cortex
- Corpus striatum
- Whats happening around you
- Ventral attentional network (engagement and activation)
- Basolateral amygdala
- Lateral and inferior frontal cortex
- temporoparietal cortex
- Ventral striatum
- how you’re going to interact
How can we diagnose confusion using the CAM diagnostic algorithm?
CAM = confusion assessment method
Diagnosis of delerium with CAM requires the presence of features 1 and 2 and either 3 or 4
- Feature 1 –> Acute onset and fluctuating course
- usually obtained from fam member/ nurse
- “is there evidence of acute change in mental status from patient’s baseline?” “has the abnormal behaviour fluctated during the day/ increase or decrease in severity?”
- Feature 2 –> Inattention
- Did pt have difficulty focussing attention e.g. being easily distractable, or having difficulty of what was being said?
- Feature 3 –> disorganised thinking
- “was the patients thinking disorganised or incoherent?”
- Feature 4 –> Altered level of conciousness
- Feature shown by any answer other than alert to the following:
- Overall how would you rate this patient’s level of conciousness? (alert, vigilant, lethargic, stupor, or coma)
What is the management of delerium?
Find and treat the underlying cause
Supportive management:
- Clear communication
- consitency of staff
- family and carer involvement
- prompts to day and time
- familiar environment
- adequate nutrition and fluids
- low stress environment
What medications can be used in the management of delerium when all other tx options have bee exhausted?
What are the risk factors for delerium?
Advanced age, advanced cancer
Underlying brain disease (dementia, stroke, parkinsons)
Organ failure (lung/ heart/kidney/liver)
Limb fracture
Immobilisation (incld. physical restraints)
Frailty, malnutrition
use of multiple medications (psychiatric drugs/ sedatives in partc.) OR multiple medical problems
suddent withdrawal of medicaiton/ cessation regular alc use
Undertreated pain
Interventions (incld. diagnostic tests)
Use of bladder catheters
Poor eyesight/ hearing
Sleep deprivation
