Poor concentration and attention difficulties

Poor concentration and attention difficulty is reduced ability to sustain focus, to shift attention, to resist distraction, or to hold and manipulate information in mind, causing errors, incomplete tasks and impaired function at work, school or home. It is a very common complaint and a nonspecific symptom.

Definitions. Attention has components: sustained attention (vigilance), selective (focused) attention, divided attention, alternating attention, and working memory with executive control.

Inattention in ADHD requires 6 or more symptoms (5 or more in people aged 17 years and over) persisting at least 6 months, present before age 12 years, in 2 or more settings, with clear impairment, and not better explained by another disorder. The symptoms are:

• careless mistakes
• difficulty sustaining attention
• not seeming to listen
• failure to finish tasks
• poor organisation
• avoidance of sustained mental effort
• losing things
• distractibility and forgetfulness

Classification by cause

• Neurodevelopmental: ADHD (predominantly inattentive or combined presentation), autism spectrum disorder, specific learning disorders, intellectual disability, foetal alcohol spectrum disorder.
• Psychiatric: depression, anxiety, bipolar disorder (including mania), posttraumatic stress disorder, psychosis, obsessive compulsive disorder, and burnout.
• Sleep related: insufficient sleep, insomnia, obstructive sleep apnoea, narcolepsy, restless legs, shift work.
• Neurological and neurocognitive: delirium, mild cognitive impairment, dementia, traumatic brain injury and concussion, epilepsy (absence seizures, nonconvulsive status), stroke, brain tumour, multiple sclerosis, Parkinson disease, hydrocephalus, long COVID and other post infectious states.
• Medical and metabolic: anaemia and iron deficiency, hypothyroidism and hyperthyroidism, diabetes (hypoglycaemia and hyperglycaemia), chronic kidney and liver disease, hyponatraemia, hypercalcaemia, vitamin B12 and vitamin D deficiency, hypoxia and heart failure, chronic infection, chronic pain, menopause, and cancer related cognitive change.
• Sensory impairment (hearing and vision loss).
• Substances and drugs: alcohol, cannabis, sedatives, opioids, anticholinergics, antihistamines, antiepileptics, benzodiazepines, antipsychotics, corticosteroids, chemotherapy, beta blockers, and withdrawal states.
• Situational: stress, grief, overwork, multitasking and screen overload.

Epidemiology. ADHD affects about 5% of children and 2.5% of adults, with persistence into adulthood in a majority, and is underdiagnosed in women and in adults. Concentration problems are reported in a majority of patients with depression and anxiety. Subjective cognitive complaints in people aged 40 to 60 years are usually due to mood, sleep, stress and drugs.

Mechanisms. Frontostriatal and fronto-parietal network dysfunction with dopamine and noradrenaline deficiency in ADHD, reduced cognitive resources in depression and anxiety, sleep loss reducing prefrontal function, diffuse neuronal dysfunction in delirium and dementia, and drug induced cholinergic or sedative blockade.

Key distinctions. Lifelong inattention with childhood onset, family history and impairment in several settings suggests ADHD. New onset inattention over weeks with low mood and loss of interest suggests depression. Acute fluctuating inattention with disorientation suggests delirium. Progressive memory loss with functional decline suggests dementia. Inattention with unrefreshing sleep, snoring and daytime sleepiness suggests sleep apnoea. Subjective difficulty with normal objective testing suggests mood, anxiety, stress or sleep disorder.

History

• Nature of the difficulty: sustaining focus, distractibility, forgetfulness, losing things, disorganisation, procrastination, missed deadlines, driving errors, and how it differs from the person's usual.
• Onset and course: lifelong, since a specific event (head injury, illness, bereavement, job change, drug start), gradual or sudden, fluctuating, and worse at a time of day.
• Childhood history: school reports, hyperactivity, impulsivity, learning difficulty, behaviour problems, family history of ADHD, and symptoms before age 12 years (collateral from a parent or old reports).
• Impairment: work, school, relationships, finances, accidents, driving violations, and unemployment.
• Mood and anxiety symptoms, mania, trauma, psychosis, obsessions, eating disorder, suicidal thoughts.
• Sleep: hours, quality, snoring, witnessed apnoeas, restless legs, shift work, naps, and daytime sleepiness.
• Substances: alcohol (AUDIT-C), cannabis, stimulants, sedatives, opioids, caffeine and nicotine, including recent stopping.
• Medical history: head injury (with loss of consciousness), epilepsy, stroke, thyroid disease, diabetes, anaemia, kidney or liver disease, HIV, cardiac disease, cancer and chemotherapy, long COVID, hearing and vision.
• Drugs: anticholinergics (oxybutynin, amitriptyline, hydroxyzine, diphenhydramine), benzodiazepines and Z drugs, opioids, gabapentinoids, antiepileptics (topiramate, phenobarbital, valproate), antipsychotics, beta blockers, corticosteroids, antihistamines, and over the counter sleep aids.
• Cognitive symptoms: memory loss, word finding difficulty, getting lost, personality change, falls, and functional decline (collateral history from a family member).
• Cardiac history before stimulant treatment: syncope, palpitations, exertional chest pain, family history of sudden death or cardiomyopathy.
• Developmental history: motor and language milestones, autism features, learning disability.
• Psychosocial: stress, caring duties, work demands, and screen use.

Examination

• Vital signs, weight and body mass index, blood pressure, pulse, oxygen saturation, and neck circumference.
• General: pallor, thyroid, signs of liver or kidney disease, signs of alcohol use, and cushingoid features.
• Neurological: orientation, attention (digit span forward and backward, months of the year backwards, serial sevens), gait, cranial nerves, visual fields, primitive reflexes, tremor, rigidity, focal signs, and cerebellar signs.
• Hearing (whisper test) and vision (acuity, visual fields).
• Mental state: mood, anxiety, thought content, psychomotor activity, insight, and suicidal thoughts.
• Bedside tests: Adult ADHD Self-Report Scale screener (6 questions, 4 or more positive suggests ADHD), the 18 item full scale, Montreal Cognitive Assessment (under 26 of 30 suggests impairment), 4AT for delirium, PHQ-9, GAD-7, Epworth Sleepiness Scale, STOP-BANG, glucose, and ECG.

Red flags

• Acute or subacute onset, fluctuating attention or disorientation (delirium).
• Head injury, loss of consciousness, vomiting, severe headache, or new focal neurological signs.
• Progressive memory loss, personality change, getting lost, falls, or functional decline in an older adult.
• Seizure, staring spells with unresponsiveness, or episodic confusion.
• Severe depression, suicidal ideation, mania, psychosis, or catatonia.
• Alcohol or drug withdrawal, or poisoning.
• Syncope, palpitations, exertional chest pain, or family history of sudden cardiac death (before stimulant treatment).
• Symptoms of hypoglycaemia, hypothyroidism, hypercalcaemia, uraemia or hepatic encephalopathy.
• Severe daytime sleepiness, falling asleep while driving, or witnessed apnoeas.
• Fever, immunosuppression, HIV, or recent travel (CNS infection).
• Visual field defect, papilloedema, or new headache pattern.
• New cognitive change in a patient on chemotherapy, steroids, anticholinergics or sedatives.
• Child with sudden decline in school performance, behaviour change, or staring spells.

Special groups

• Children and adolescents: assess teachers' reports, learning disorders, vision, hearing, sleep, anxiety, trauma and autism. Use age specific doses.
• Women: ADHD is under recognised and inattentive presentations are common. Menstrual cycle, perimenopause and pregnancy affect symptoms.
• Pregnancy: avoid starting stimulants unless benefit outweighs risk. Assess anaemia, thyroid disease and sleep.
• Older adults: first exclude delirium, depression, drug effects, sensory loss and sleep apnoea before diagnosing mild cognitive impairment.
• Chronic illness and cancer: drugs, anaemia, pain, sleep loss, mood and direct effects of disease.
• Region specific: malnutrition, iron deficiency, malaria and cerebral infection, HIV related disorders, lead exposure, khat and alcohol use.

Neurodevelopmental and psychiatric

• Attention deficit hyperactivity disorder (inattentive, combined).
• Autism spectrum disorder and specific learning disorders.
• Intellectual disability and foetal alcohol spectrum disorder.
• Major depressive disorder and persistent depressive disorder.
• Generalised anxiety disorder, panic disorder and social anxiety disorder.
• Bipolar disorder (mania, hypomania, depression).
• Posttraumatic stress disorder and acute stress disorder.
• Psychotic disorders (prodrome and negative symptoms).
• Obsessive compulsive disorder (intrusive thoughts consuming attention).
• Burnout and adjustment disorder.
• Eating disorders and substance use disorders.

Sleep and circadian

• Insufficient sleep, insomnia disorder and shift work disorder.
• Obstructive sleep apnoea and obesity hypoventilation.
• Narcolepsy and idiopathic hypersomnia.
• Restless legs syndrome and periodic limb movements.
• Delayed sleep phase disorder.

Neurological and cognitive

• Delirium.
• Mild cognitive impairment, Alzheimer disease, vascular cognitive impairment, Lewy body dementia and frontotemporal dementia.
• Traumatic brain injury and postconcussion syndrome.
• Epilepsy, including absence and complex partial seizures, and nonconvulsive status epilepticus.
• Stroke, brain tumour, normal pressure hydrocephalus and subdural haematoma.
• Multiple sclerosis, Parkinson disease and Huntington disease.
• Encephalitis, HIV associated neurocognitive disorder, neurosyphilis and cerebral malaria.
• Long COVID cognitive impairment.
• Chronic migraine and chronic fatigue syndrome.

Medical and metabolic

• Anaemia and iron deficiency.
• Hypothyroidism and hyperthyroidism.
• Diabetes mellitus (hypoglycaemia, hyperglycaemia).
• Hyponatraemia, hypercalcaemia and hypomagnesaemia.
• Chronic kidney disease and uraemia; chronic liver disease and hepatic encephalopathy.
• Vitamin B12, folate, thiamine and vitamin D deficiency.
• Hypoxia, heart failure, COPD and hypercapnia.
• Adrenal insufficiency and Cushing syndrome.
• Systemic lupus erythematosus and other autoimmune disease.
• Cancer related cognitive impairment, paraneoplastic syndromes.
• Menopause and hormonal change.
• Hearing and vision loss.
• Lead and other heavy metal toxicity, and carbon monoxide poisoning.

Substances and drugs

• Alcohol use, hangover and withdrawal.
• Cannabis, benzodiazepine, opioid and stimulant use or withdrawal.
• Anticholinergic burden (tricyclic antidepressants, oxybutynin, first generation antihistamines).
• Benzodiazepines, Z drugs, gabapentinoids, antiepileptics (topiramate, phenobarbital), antipsychotics, beta blockers, corticosteroids, chemotherapy and immunotherapy.
• Caffeine excess and nicotine withdrawal.

Step 1. Exclude acute causes. Check vital signs, glucose, oxygen saturation and level of consciousness. Screen for delirium (4AT) in any acute change. Examine for head injury and focal signs. Treat intoxication and withdrawal.

Step 2. Characterise the problem. Obtain a developmental history and collateral report for ADHD, a cognitive history and informant report (for example the AD8 informant questionnaire, a score of 2 or more suggests cognitive impairment) for dementia, and a 2 week sleep diary. Rate current symptoms with the Adult ADHD Self-Report Scale and, in specialist settings, a structured interview (DIVA-5). Screen for depression, anxiety, bipolar disorder, trauma, alcohol and drugs.

Step 3. First line tests

• Full blood count, ferritin, urea, creatinine, electrolytes (sodium), calcium, glucose or HbA1c, liver tests, thyroid stimulating hormone, vitamin B12 and folate, and CRP.
• Urine or serum drug screen when substance use is suspected.
• HIV and syphilis serology where risk exists.
• Pregnancy test in women of reproductive age.
• 12 lead ECG and blood pressure before stimulant or atomoxetine treatment, with further cardiac assessment if there are cardiac symptoms or family history of sudden death.
• Hearing and vision tests.

Step 4. Targeted tests

• Cognitive testing: Montreal Cognitive Assessment or Addenbrooke Cognitive Examination, then neuropsychological testing for attention, working memory and executive function (continuous performance tests) when diagnosis is unclear.
• CT or MRI brain for focal signs, head injury, progressive decline, headache, seizures, age over 60 years with new cognitive change, or atypical features.
• Electroencephalogram for staring spells, fluctuating consciousness or suspected seizures.
• Polysomnography or home sleep apnoea testing for sleep apnoea; multiple sleep latency test for suspected narcolepsy.
• Lumbar puncture and autoimmune antibodies when encephalitis is suspected.
• Lead level in children and exposed adults, and vitamin D, cortisol, testosterone and parathyroid hormone as directed.
• Formal assessment for autism and learning disorder when features are present.

Step 5. Interpretation. Diagnose ADHD only when symptoms began in childhood, are present in several settings, cause impairment, and are not better explained by another disorder, after treatment of coexisting depression, anxiety and sleep disorder. Coexisting conditions are common in ADHD (depression, anxiety, substance use, autism), and all need treatment. Normal cognitive testing with high subjective complaint points to mood, stress or sleep as the cause.

Limits. Self report scales are not diagnostic. Neuropsychological tests are affected by effort, mood and sleep. Childhood symptoms are recalled imperfectly, so collateral information helps. ADHD is a clinical diagnosis with no biomarker.

Immediate. Treat any acute cause (delirium, hypoglycaemia, intoxication, withdrawal). Assess suicide risk if mood is low. Advise on driving and safety-critical work when attention is impaired. Provide explanation and a plan for investigation.

General measures for all patients

• Treat and optimise sleep (regular schedule, 7 to 9 hours, avoid late caffeine and alcohol), regular exercise (30 minutes on most days), balanced meals, and reduction of caffeine to under 200 mg daily and of alcohol, cannabis and nicotine.
• Practical strategies: lists, calendars and reminders, task chunking, timers, reduced multitasking and screen distraction, quiet workspace, scheduled breaks, and body doubling.
• Workplace and school adjustments (extra time, written instructions, regular supervision, quiet space).
• Mindfulness based training and coaching may help. Computerised cognitive training has limited evidence.

Treatment of the cause

• Iron deficiency: ferrous sulphate 200 mg (65 mg elemental iron) orally once daily or on alternate days for 3 months after haemoglobin normalises, or intravenous ferric carboxymaltose 500 to 1000 mg once when oral iron fails.
• Vitamin B12 deficiency: hydroxocobalamin 1 mg intramuscularly on alternate days for 2 weeks, then every 3 months (neurological involvement: 1 mg on alternate days until no further improvement, then every 2 months).
• Hypothyroidism: levothyroxine 1.6 micrograms/kg orally once daily on an empty stomach in healthy adults (25 to 50 micrograms daily in older adults and heart disease, increased every 4 to 6 weeks), monitored by thyroid stimulating hormone at 6 to 8 weeks.
• Hyperthyroidism: carbimazole 15 to 40 mg daily with propranolol 10 to 40 mg three or four times daily until euthyroid.
• Depression and anxiety: psychological therapy and sertraline 50 mg daily (25 mg for the first week if anxious) increased to 50 to 200 mg, or escitalopram 10 mg daily (maximum 20 mg; 10 mg over 65 years). Vortioxetine 10 mg daily (maximum 20 mg) may help cognition.
• Sleep apnoea: continuous positive airway pressure (auto titrating 4 to 20 cmH2O), weight loss and positional therapy. Insomnia: cognitive behavioural therapy for insomnia.
• Diabetes: correct hypoglycaemia and optimise glycaemic control. Hyponatraemia, hypercalcaemia and uraemia: treat by cause.
• Drug induced: reduce or stop anticholinergics, sedatives, benzodiazepines and other offending drugs where possible, with slow taper of dependence forming drugs.
• Traumatic brain injury and concussion: relative rest for 24 to 48 hours, graded return to activity, sleep, headache treatment, and rehabilitation.
• Alcohol and substance use: brief intervention and addiction treatment.
• Cognitive impairment and dementia: cognitive rehabilitation, vascular risk control.
• For Alzheimer disease and Lewy body dementia: donepezil 5 mg daily increasing to 10 mg after 4 to 6 weeks, or rivastigmine 1.5 mg twice daily increasing every 2 to 4 weeks to 3 to 6 mg twice daily.
• For moderate to severe disease: memantine 5 mg daily increasing weekly to 20 mg daily (reduce to 10 mg daily at creatinine clearance 5 to 29 mL/min). Check pulse and ECG before cholinesterase inhibitors.
• Epilepsy: antiepileptic drug by seizure type, avoiding agents that impair cognition (topiramate, phenobarbital).
• Hearing and vision loss: correction with hearing aids, cataract surgery and glasses.

Pharmacological treatment of ADHD in adults (after confirmed diagnosis; specialist initiation and review)

• Cardiovascular check before starting: blood pressure, pulse, ECG if cardiac history, and baseline weight. Contraindications: uncontrolled hypertension, symptomatic cardiovascular disease, arrhythmia, hyperthyroidism, phaeochromocytoma, glaucoma, current psychosis or mania, substance dependence with misuse risk, concurrent monoamine oxidase inhibitor (washout 14 days).
• Methylphenidate immediate release 5 mg orally 2 to 3 times daily, increased weekly by 5 to 10 mg daily to a usual 30 to 60 mg daily in 2 to 3 divided doses (maximum 100 mg daily in specialist care).
• Methylphenidate modified release forms: 18 mg once daily in the morning, increased by 18 mg weekly to 36 to 72 mg (maximum 108 mg daily for adults in some settings).
• Methylphenidate side effects: reduced appetite, insomnia, headache, anxiety, raised blood pressure and pulse, tics, rare psychosis.
• Lisdexamfetamine 30 mg orally once daily in the morning, increased by 20 mg at weekly intervals to 50 to 70 mg (maximum 70 mg daily). Reduce the maximum at creatinine clearance 15 to 30 mL/min (50 mg) and under 15 mL/min (30 mg).
• Dexamfetamine 5 mg orally twice daily, increased weekly to 20 mg daily (maximum 60 mg daily in specialist care).
• Atomoxetine 40 mg orally once daily for 7 days, then 80 mg daily, increasing after 2 to 4 weeks to a maximum of 100 mg daily.
• Atomoxetine dose adjustment: adjust in hepatic impairment: halve in moderate, quarter in severe impairment, and with CYP2D6 inhibitors such as paroxetine and fluoxetine.
• Atomoxetine onset takes 4 to 6 weeks. Monitor blood pressure, pulse, liver injury symptoms and suicidality.
• Guanfacine extended release (adults: off label) 1 mg orally daily, increased by 1 mg weekly to 4 to 7 mg daily, and bupropion extended release 150 mg daily increased to 300 mg (off label, alternative when stimulants are unsuitable).
• Response: review at 1 to 2 weeks after each dose change, then at 4 to 6 weeks with a symptom scale (ASRS, Conners). Titrate to benefit, and stop if no clear benefit after adequate dose. Monitor blood pressure and pulse (before each dose change, every 3 to 6 months), weight, sleep, appetite, mood, misuse, and cardiovascular symptoms.
• Psychological treatment: cognitive behavioural therapy for adult ADHD (group or individual, 12 to 16 sessions), psychoeducation, coaching, and skills training. Combine with drugs for moderate to severe disease.

Special populations

• Pregnancy and breastfeeding: stop or reduce stimulants where possible after risk and benefit discussion. Use nonpharmacological measures.
• Children and adolescents: use age specific treatment through paediatric services (behavioural parent training under 5 years, medication from 6 years).
• Older adults: look for delirium, dementia, depression, drugs and sensory loss. Stimulants need cardiac assessment.
• Kidney and liver impairment: lowest effective dose, and avoid atomoxetine in severe hepatic impairment.
• Comorbid substance use: prefer long acting formulations or atomoxetine and monitor misuse.

Monitoring. Symptom scale scores, function at work or school, blood pressure and pulse, weight, sleep, mood, suicidal thoughts, substance use, adverse effects, adherence, and repeated cognitive testing at 6 to 12 months in suspected dementia.

Referral and escalation. Psychiatry or ADHD specialist services for diagnostic uncertainty, comorbidity, treatment failure and drug initiation. Neurology for seizures, head injury, progressive decline and neurological signs. Old age psychiatry or memory clinic for suspected dementia. Sleep medicine, endocrinology, cardiology as indicated. Neuropsychology for complex assessment. Educational and occupational support services.

Admission criteria. Delirium, acute neurological emergency, severe depression with suicidal intent, mania or psychosis, and withdrawal needing inpatient care.

Discharge and follow up. Written plan and explanation, driving and safety advice, review in 4 to 6 weeks, then every 3 to 6 months. Safety net advice: return for new confusion, severe headache, seizure, falls, suicidal thoughts, chest pain or palpitations on stimulants, high fever, or rapidly worsening cognition.