Latest news with #neurology
ABC News
2 days ago
- Health
- ABC News
Scientist holding a donated brain
Australian scientists have found the first evidence of an unusual pattern of brain scarring only seen in people repeatedly exposed to blast waves.
Medscape
2 days ago
- Health
- Medscape
Uncontrolled Movements, Anger, and Insomnia
Editor's Note: The Case Challenge series includes difficult-to-diagnose conditions, some of which are not frequently encountered by most clinicians, but are nonetheless important to accurately recognize. Test your diagnostic and treatment skills using the following patient scenario and corresponding questions. If you have a case that you would like to suggest for a future Case Challenge, please email us at ccsuggestions@ with the subject line "Case Challenge Suggestion." We look forward to hearing from you. Background A 35-year-old man presents to the neurology clinic due to abnormal movements over the past 6 years. The involuntary movements began in the right upper limb, followed sequentially by the left upper limb, left lower limb, and finally the head and neck. The movements occur during wakefulness and are absent in sleep. They are described as jerky and nonpurposeful. His gait has assumed a dancelike character. He also has had behavioral changes that include frequent outbursts of anger, aggressive behavior, depressive mood, and insomnia. His abnormal movements are aggravated during outbursts of anger and disturbances in mood. He has no weakness in any limbs but is unable to perform regular household activities. Family members have also noted memory impairment. He has been unable to continue his work as a machine operator for the past 3 months. He has no history of psychoactive drug intake, including phenytoin, phenothiazines, haloperidol, L-dopa, lithium, isoniazid, amphetamines, tricyclic antidepressants, or any other relevant drugs. He reports no history of chest pain, breathlessness, or joint pain. His family history includes a paternal grandfather and father who had similar forms of abnormal movements and died at the age of 60 years and 55 years, respectively. The patient has five siblings (two brothers, three sisters). His elder brother died by suicide at age 25 years, and his elder sister died at age 33 years. Both had abnormal movements and abnormal behaviors. One of his younger sisters (age 22 years) also has similar abnormal movements and depressed attitude. His younger brother (age 17 years) and other younger sister (age 14 years) are healthy and symptom-free. The patient's children, an 8-year-old son and a 10-year-old daughter, are symptom-free. His past medical history is positive for hypertension, which is well controlled with lisinopril (20 mg daily). He has no surgical history. He does not smoke, drink, or use recreational drugs. Physical Examination and Workup A general examination reveals a pleasant man who is well built and in no acute distress. His blood pressure is 140/80 mm Hg, his heart rate is 78 beats/min, his respiratory rate is 12 breaths/min, his SpO 2 level is 98% on room air, and his body mass index (BMI) is 20. He is afebrile. A cardiovascular examination reveals normal peripheral pulses and normal heart findings. A chest examination reveals normal auscultation and expansion. His abdomen is soft. Head, eyes, ears, nose, and throat (HEENT) examination findings are unremarkable. He does not have a skin rash. A visual examination reveals normal acuity, field, and fundi. His affect is flat. A neurologic examination of the higher mental functions reveals that the patient is awake and alert, with normal orientation, attention, concentration, fund of knowledge, and language function. His memory is impaired, with recall one-third at 3 minutes. He has a normal past memory. His speech is normal. A cranial nerve examination reveals normal extraocular movements, increased blink rate, normal facial sensation, a symmetric face with abnormal fidgety movement, normal hearing, and normal palate movement. He has abnormal tongue movement and cannot protrude his tongue more than 20 seconds (darting tongue movement). He has normal shoulder shrug. No Kayser-Fleischer ring is noted during slit-lamp examination. An examination of the motor system reveals decreased muscle tone, normal bulk, and 5/5 strength in both upper and lower extremities. No atrophy or fasciculation is noted. Deep tendon reflexes are normal (2+ with flexor planters). Sensory examination findings are normal. Finger-nose test findings are normal. An examination of the extrapyramidal system reveals reduced tone and involuntary choreoathetoid movements that affect both upper and lower extremities as well as his face. He has a dancing gait. Diagnostic tests reveal normal complete blood cell count (CBC) and comprehensive metabolic panel findings. He has normal serum findings and urine copper levels. His erythrocyte sedimentation rate (ESR) is 22 mm/hr (reference range, 0-22 mm/hr). He has normal ECG findings, a normal thyroid-stimulating hormone (TSH) level, a normal transthoracic echo (with ejection fraction 65%), and normal chest radiography findings. Brain MRI can be used to evaluate for selective atrophy of deep gray structures, to document disease burden, and to provide a baseline for future comparison. Whole-body 18-FDG PET/CT may be used to screen for occult neoplasm and paraneoplastic chorea, but this is exceedingly rare and typically subacute. NMDA receptor antibody panel may be used to investigate for autoimmune encephalitic chorea, but the features of this (ie, seizures, psychosis, and autonomic instability) are absent in this case. RPR and FTA-ABS may be used to evaluate for neurosyphilitic chorea, but this is also very uncommon and unnecessary without risk factors or acute symptoms. In this patient, brain MRI reveals evidence of bilateral caudate atrophy, with increased intercaudate distance (Figure). Figure. Cerebrospinal fluid (CSF) examination findings are normal. Discussion This 35-year-old man has Huntington disease. He has insidious-onset, slowly progressive movement disorder, and movements are absent during sleep. His movements are described as choreoathetoid. He has family history that suggests autosomal dominant transmission. Apart from the movement disorder, he also has neuropsychiatric manifestations, with death at an early age in the family. A CT scan of the head revealed evidence of caudate nucleus atrophy. Brain MRI revealed evidence of caudate atrophy (Figure). Figure. In evaluating the differential diagnoses, the patient has no history of antipsychotic medication use to suggest tardive dyskinesia. He has no clinical or diagnostic evidence of infection or heart involvement, which makes Sydenham chorea unlikely. No acanthocytes were observed, helping to exclude neuroacanthocytosis. The strong family history of progressive abnormal movements and neuropsychiatric symptoms across generations supports a genetic etiology, specifically autosomal-dominant Huntington disease. Huntington disease is a rare neurodegenerative disorder of the central nervous system (CNS) characterized by choreiform movements, behavioral and psychiatric disturbances, and dementia.[1] Huntington disease is caused by an autosomal-dominantly inherited expansion of CAG trinucleotide repeats in the huntingtin ( HTT ) gene on chromosome 4; this leads to production of a mutant huntingtin (mHTT) protein, with an abnormally long polyglutamine repeat.[2] Individuals with more than 39 CAG repeats develop the disease, whereas reduced penetrance is seen in those with 36-39 CAG repeats. The disease can be anticipated when the gene is passed down the paternal line, as in this case; a father with a CAG repeat length in the intermediate range may have a child with an expanded pathogenic repeat length. This is because sperm from males shows greater repeat variability and larger repeat sizes than somatic tissues. Mutant huntingtin protein leads to death and neuronal dysfunction through various mechanisms. Postmortem studies reveal diffuse atrophy of the caudate and putamen. The progressive worsening of Huntington disease leads to a bedridden state with cognitive deterioration, and death typically occurs about 20 years after the onset of symptoms.[3] Prevalence in the white population is estimated at 1 in 10,000 to 1 in 20,000. The mean age at symptom onset is 30-50 years. In some cases, symptoms begin before age 20 years, with behavior disturbances and learning difficulties at school; this is termed juvenile Huntington disease (Westphal disease).[4] The first description, by Waters, dates to 1842. However, after a description in 1872 by George Huntington, it became known as Huntington chorea. In 1983, a linkage on chromosome 4 was established, and in 1993 the gene for Huntington disease was found.[1] Diagnosis of Huntington disease is confirmed by demonstration of autosomal dominant transmission or gene testing in the presence of clinical features.[5] The clinical features of Huntington disease consist of motor, cognitive, and neuropsychiatric manifestations. Huntington disease has a biphasic course of hyperkinetic phase with chorea in the early stages of disease that then plateaus into a hypokinetic phase, consisting of bradykinesia dystonia, balance issues, and gait disturbance. The younger-onset variant is associated with predominant bradykinesia.[6] Cognitive disturbance can be seen many years before other symptom onset and is characterized by impaired emotion recognition, processing speed, and executive function abnormality. Neuropsychiatric symptoms widely vary, including apathy, anxiety, irritability, depression, obsessive-compulsive behavior, and psychosis. A lack of awareness of early and progressing behavioral, cognitive, and motor symptoms is a hallmark of Huntington disease. This unawareness is caused by the disease itself (specifically, impaired insight or anosognosia) and is not the result of intentional denial, avoidance, or suppression of symptoms.[7] Therefore, a comprehensive history, including information from a knowledgeable family member/caregiver, is advisable.[7] Numerous conditions can mimic Huntington disease, including a spinal cerebellar ataxia 17, spinocerebellar ataxia 1-3, and Friedreich ataxia, which involve neuropathy. If seizures are also present, dentatorubropallidoluysian atrophy should be considered. Acanthocytes are seen in patients with neuroacanthocytosis.[8-10] Isolated chorea can be seen in acquired conditions, including chorea gravidarum, systemic lupus erythematosus, antiphospholipid syndrome, thyrotoxicosis, postinfectious syndromes, polycythemia vera, and some drug use. Genetic testing for the mHTT mutation can be either diagnostic or predictive.[6] A diagnostic test may be performed when a patient presents with typical motor features of Huntington disease. Prior to testing, the patient should be informed about Huntington disease and its hereditary nature, as a positive test result has implications for the patient and family. Predictive testing is performed in asymptomatic patients, mostly for reproductive reasons. Treatment of Huntington Disease The optimal management of Huntington disease involves a multidisciplinary approach that includes neurology, nurses, physical therapy, speech-language pathology, and dietitians and other healthcare professionals. The goal is to optimize the quality of life based on the changing need of the patient. These consist of combined pharmacologic and lifestyle changes, including behavioral therapy. Symptoms may be worsened by stress, fatigue, and intercurrent disorders (eg, anxiety, digestive disorders, infectious or painful conditions), so these aspects must be assessed and treated alongside the primary symptoms of Huntington disease.[3] In clinical practice, information about symptoms should be obtained from both the patient and caregivers, since patients may have impaired awareness of their condition.[11] Identifying coexisting psychiatric symptoms, comorbid medical conditions, and environmental factors is crucial.[11] Educating caregivers about the nature and presentation of symptoms and methods to modify triggers is also vital.[11] Medication choices should be guided by coexisting symptoms and disease stage, and regular reassessment of drug need and potential for dose reduction is important because of adverse effects that can mimic disease progression.[11] Nonpharmacologic interventions, including behavioral therapies and environmental modifications, should be prioritized for neuropsychiatric symptoms in Huntington disease. Pharmacologic agents may be considered if these measures are insufficient, and consultation with a psychiatrist knowledgeable in Huntington disease is recommended for individuals whose symptoms are resistant to standard pharmacologic therapy.[11] Tetrabenazine and its modified version, deutetrabenazine, are commonly used to treat choreiform movements. Side effects of tetrabenazine can include depression, anxiety, sedation, sleep problems, restlessness, and parkinsonism.[7] Citalopram is a selective serotonin reuptake inhibitor used to manage depression. Modafinil and atomoxetine are used to manage apathy. Tiapride, although unavailable in the United States, is considered a first-line treatment option for chorea outside the United States.[7] Other antipsychotics such as olanzapine, risperidone, and quetiapine are also used to manage chorea. Risperidone may also help with psychomotor restlessness, and olanzapine and quetiapine can have additional benefits like weight gain (which can be desirable in Huntington disease) and mood stabilization. Haloperidol has also shown effectiveness.[7] Medications used to suppress chorea (eg, tetrabenazine and deutetrabenazine and certain antipsychotics) should be used sparingly and mainly for subjectively disabling hyperkinesias, starting at low doses and titrating gradually. They make take 4-6 weeks to show results.[7] The choice of medication depends on the individual patient's symptoms, tolerability, and co-existing conditions.[7] Evidence regarding the treatment of psychiatric symptoms in Huntington disease is limited, with recommendations often based on expert opinion owing to a lack of robust controlled studies.[7,11] Nonpharmacologic interventions such as cognitive-behavioral therapy and psychodynamic therapy are recommended, especially for depression, anxiety, obsessive-compulsive behaviors, and irritability. Behavioral strategies (eg, structured routines and distraction) are important for managing irritability and agitation.[3,11] Depression: Selective serotonin reuptake inhibitors (SSRIs) such as citalopram, fluoxetine, paroxetine, sertraline, and venlafaxine are recommended as pharmacologic options. [3,7] Mianserin (unavailable in the United States) or mirtazapine are alternatives, particularly in patients with sleep disruption. [3,7,11] Electroconvulsive therapy (ECT) may be considered for severe or resistant cases, although it can significantly impair short-term memory. [3,7] Mianserin (unavailable in the United States) or mirtazapine are alternatives, particularly in patients with sleep disruption. Electroconvulsive therapy (ECT) may be considered for severe or resistant cases, although it can significantly impair short-term memory. Anxiety: SSRIs or serotonin-noradrenaline reuptake inhibitors (SNRIs) are first-line treatments, especially when anxiety coexists with depression. [3,11] Mirtazapine is an option in patients with sleep disorders. [11] Long-term use of benzodiazepines is generally discouraged for ambulatory individuals because of the risk of falls and dependence but can be used short-term or as needed. [3,11] Mirtazapine is an option in patients with sleep disorders. Long-term use of benzodiazepines is generally discouraged for ambulatory individuals because of the risk of falls and dependence but can be used short-term or as needed. Obsessive-compulsive behaviors/perseverations: For true obsessive-compulsive phenomena, SSRIs are considered first-line treatment. [3] Olanzapine and risperidone may also be valuable for ideational perseverations, particularly if associated with irritability. [3] Clomipramine is an option, especially if needed for coexisting obsessive perseverative behaviors. [11] Olanzapine and risperidone may also be valuable for ideational perseverations, particularly if associated with irritability. Clomipramine is an option, especially if needed for coexisting obsessive perseverative behaviors. Irritability and aggression: SSRIs are a first-line treatment. [3] For aggressive behavior, neuroleptics are recommended. [3,7] Mood stabilizers (eg, valproate, lamotrigine, lithium, carbamazepine) can be added if irritability is resistant to other treatments or for mood lability. Risperidone and olanzapine may help reduce irritability. [3,7] For aggressive behavior, neuroleptics are recommended. Mood stabilizers (eg, valproate, lamotrigine, lithium, carbamazepine) can be added if irritability is resistant to other treatments or for mood lability. Risperidone and olanzapine may help reduce irritability. Psychosis (hallucinations/delusions): Second-generation neuroleptics (antipsychotics) are the first-line pharmacologic treatment. [3,7,11] Options include olanzapine, risperidone, quetiapine, aripiprazole, and haloperidol. [7] Clozapine may be considered for severe or resistant cases, particularly in akinetic forms of Huntington disease but requires regular monitoring. [3,7,11] Underlying causes, such as the use of psychotropic agents or somatic triggers, should be investigated and addressed. [3,11] Options include olanzapine, risperidone, quetiapine, aripiprazole, and haloperidol. Clozapine may be considered for severe or resistant cases, particularly in akinetic forms of Huntington disease but requires regular monitoring. Underlying causes, such as the use of psychotropic agents or somatic triggers, should be investigated and addressed. Apathy: Personalized cognitive stimulation and structured routines and activities are recommended.[3,7,11] If depression is suspected as a contributor, an SSRI should be tried.[3,11] In patients without depression, activating antidepressants or stimulant drugs (eg, methylphenidate, atomoxetine, modafinil) may be considered.[11] Sedative medications may increase apathy, so their dosage should be monitored or reduced.[3,11] Currently, no pharmacological treatment is specifically recommended for cognitive symptoms in Huntington disease.[3,7] Rehabilitation strategies, including speech therapy, occupational therapy, cognitive and psychomotor therapy, may help transiently improve or stabilize cognitive functions.[3,7] Coping strategies can be useful as an alternative to medication. Certain medications, such as sedative drugs, neuroleptics, and tetrabenazine, can negatively affect memory, executive functions, and attention.[3] Apart from symptomatic treatment, pharmacologic agents have failed to show benefit in clinical trials as disease-modifying agents. The most promising approaches in regard to disease modification are emerging therapies aimed at lowering levels of mHTT by targeting either the DNA or RNA of the mHTT gene.[12] RNA-targeting using antisense oligonucleotides (ASOs) have shown disappointing results in clinical trials. This has shifted significant research focus and toward orally available small molecules that modify HTT mRNA splicing, thereby reducing mHTT protein production. DNA-targeting approaches using gene editing tools like CRISPR/Cas9, while demonstrating success in preclinical models, remain in the early stages of development.[13,14] The patient in this case was diagnosed with Huntington disease with CAG repeat 78. He was started on tetrabenazine for abnormal movements and citalopram for depression. He opted to apply for federal disability. His children are asymptomatic, and the family decided not to investigate until symptoms develop or they are age 18 years.
Daily Mail
6 days ago
- Health
- Daily Mail
EXCLUSIVE A doctor laughed in my face when I said I felt like a ghost was touching my body - then a life-changing diagnosis explained everything
I'd always imagined that if I was told that I had a serious illness I'd feel shocked, scared and afraid. What I hadn't expected was that I'd also feel relieved. In 2001, I was spinning. I was about to turn 30 and had recently left a long, abusive relationship. I had a new job, had just moved home and my stress levels were rocketing. It was no wonder that I felt ill. It began with creeping fatigue that made my brain feel foggy, like I'd been day drinking and left me wanting to crawl into bed the moment I got back to my flat. I also felt queasy and dizzy at times. Then the ghostly symptoms started. I had a strange sensation like someone invisible was gripping my left arm and foot along with a tickling feeling on my nose and tongue. It was like a hand running down my face. Sometimes I'd jump because it felt like someone had thrown a tennis ball at my calf. I felt embarrassed describing this to anyone because it sounded so bizarre and like I needed an exorcism. The GP referred me to a neurologist who sent me for a load of tests, suggesting that we needed to make sure this wasn't multiple sclerosis, a chronic disease that affects the central nervous system. I was a nurse and the only people I'd met who had MS had advanced disease and were restricted in their mobility, often unable to get out of bed and needing care to go about their daily lives. The words 'multiple sclerosis' set off a reel of scary, negative images in my head and I felt totally panicked - but it was a huge relief when a letter came from the hospital saying that the MRI scan of my brain didn't show any of the scarring that you'd expect to see in MS. With time, the symptoms gradually resolved, but would come back if I was tired or under the weather. I'd tell myself to relax and try to ignore it, putting it all down to stress. I didn't know many nurses who weren't under pressure - it came with the job. Then in 2005, I woke up and staggered to the kitchen, noticing that I had almost no vision in my left eye. The hospital doctor was abrupt and didn't say much until he examined me. Then, he softened his tone and I guessed bad news was coming. He told me that my eye showed inflammation that is seen in people with MS but we needed another MRI scan to confirm this. Suddenly, it felt like I was back in the horror movie once again. On a subsequent appointment a more empathetic doctor took the time to reassure me and explained that MS is a complex spectrum illness that can present in many ways. Because of where I worked, I'd only met people with MS who were having more extreme problems and needed hospitalisation. My vision came back after a couple of months and I tried to push the thoughts of what might be wrong with me to the back of my mind. Bafflingly, the MRI came back negative and there was no explanation given of what caused me to go temporarily blind. I was relieved but puzzled. It took another 14 years before there was confirmation that I actually had MS. I started a strange merry-go-round of health and illness where I'd become more stable, feel almost normal and then the same weird symptoms would start again along with a few new ones. I ricocheted between neurologists, having a handful more MRI scans, saw my GP countless times and made a raft of excuses to myself about what was going on with me. Wanting to lie down in the aisle of the supermarket because I was so overwhelmingly tired? Isn't everyone exhausted these days? Numb patches on my body? I was imagining them and was hysterical so they were best ignored. Constant nausea? It was nerves - life is stressful after all. I decided that maybe I was just a hypochondriac with a vivid imagination - it was an argument that held up for many, as people lost patience with me at times. I'd cancel events because I needed to sleep (yet still woke up feeling exactly as tired), received strange looks if I mentioned any symptoms, and would pass off the occasional limp as 'just a thing I've always done.' My partner tried to understand but without a name for what was wrong with me it wasn't easy. A family member even said to my face that they thought the illness was all 'imaginary'. The health professionals weren't always much better. The neurologists would be interested in me when they examined me and heard my history - but as soon as the MRI scans showed no scarring they'd send a letter discharging me back to the care of the GP. One doctor even laughed in my face once and said that he thought they needed to name 'a special little syndrome' after me. That one smarted. I learned to keep quiet and fake wellness when I could. In 2020, I noticed that my left foot was numb and over a few days the reduced sensation crept up to my rib cage. At that point used to dismissing myself, I limped around for a week with a half numb left side, going to work in my job as a palliative care nurse specialist, passing it off as a sprain or back injury. But when I finally went to A and E and was scanned they found the scarring in my brain and spine that they'd looked for over the past almost two decades. The panic and fears for the future were the first emotions to rise to the surface - but I also realised that now I had a name for my illness, things might change. People would maybe stop judging me, labelling me as a hypochondriac and showing lack of empathy. It was a relief - and validating - to know that I had an illness with a name that people had heard of. I'm now on treatment (a monthly injection that won't change the existing scarring to my nervous system but is trying to prevent further damage) and had to give up my job as a nurse after thirty years; due to the fatigue, numbness and chronic pain. My specialist doctor thinks that it's likely that I had MS from the first attack nineteen years before but that the scars were small and because the scans were always done as non-urgent, months after the attacks, the swelling had gone down making them harder to see. I decided to channel my experience into something bigger, choosing to turn to something I'd always enjoyed - writing. As a fan of crime fiction specifically, it occurred to me to upend the classic psychological thriller story by creating a character with a neurological illness - who is driven to contemplating a crime. Like me, my main character is often disbelieved, devalued and tries to hide her illness. I've been staggered and heartened by the positive response the book has had from readers with chronic illnesses. I always joke that despite our symptoms, we can still participate in life on better days - and even commit ghastly crimes if we want to - but I'm not planning on this myself of course, nor advocating it for others. The diagnosis has also led to another new facet of my life - community. The other day, a friend who has a post-viral fatigue syndrome mentioned how much they were struggling with the hot weather. Heat often flares up chronic illness and I replied that my MS symptoms had too surfaced with the sunnier skies. She responded by devaluing herself and saying that MS is, of course, in a different league. I disagreed. Illness is illness, whether it has a name or not and suffering can be equal. There's no hierarchy just because of an illness name. Lots of people have a thing called functional neurological disorder where they have disabling symptoms that present like MS, epilepsy or Parkinson's disease yet never have any organic evidence of illness. It's not a choice, nor hypochondria nor hysteria. It's a recognised illness that should be treated with kindness. I don't feel bitter that it took so long to have a diagnosis and it wouldn't have changed the treatment I'd have had at the time. Treatments for MS have advanced considerably and continue to do so. However, what I do wish is that someone had taken the time to explain what might be wrong and that I hadn't felt so judged and alone. Maybe if I'd known I had MS for all that time I'd have worried more but equally, I'd have felt less like I was going mad. As it is, I'm managing to live with the ghosts with their strange grip on my limbs and their tennis ball throwing. I'm writing crime thrillers when I can do it around the crippling fatigue and trying to life the best life I can. Chris Bridge's latest book Sick To Death came out on 27 March. WHAT IS MULTIPLE SCLEROSIS? Multiple sclerosis (known as MS) is a condition in which the immune system attacks the body and causes nerve damage to the brain and spinal cord. It is an incurable, lifelong condition. Symptoms can be mild in some, and in others more extreme causing severe disability. MS affects 2.3 million people worldwide - including around one million in the US, and 100,000 in the UK. It is more than twice as common in women as it is in men. A person is usually diagnosed in their 20s and 30s. The condition is more commonly diagnosed in people of European ancestry. The cause isn't clear. There may be genes associated with it, but it is not directly hereditary. Smoking and low vitamin D levels are also linked to MS. Symptoms include fatigue, difficulty walking, vision problems, bladder problems, numbness or tingling, muscle stiffness and spasms, problems with balance and co-ordination, and problems with thinking, learning and planning. The majority of sufferers will have episodes of symptoms which go away and come back, while some have ones which get gradually worse over time. Symptoms can be managed with medication and therapy. The condition shortens the average life expectancy by around five to 10 years.
Health Line
6 days ago
- Health
- Health Line
What Happens During a Migraine Diagnosis?
Key Takeaways A migraine diagnosis involves gathering your medical history, performing a physical exam, and possibly ordering scans to rule out other conditions. Migraine symptoms include severe head pain, throbbing, and sensitivity to light, sound, and smells. They can be preceded by warning signs like mood changes or visual disturbances. Treatment focuses on stopping symptoms with medication and preventing future episodes by identifying triggers and using preventative medications or therapies. Migraine can disrupt your entire day. Frequent migraine attacks can disrupt your life and make it difficult for you to work, spend time with family, or do everyday activities. Thankfully, getting diagnosed with migraine can give you the tools to help reduce or even eliminate your migraine attacks and their symptoms. Getting diagnosed can sometimes happen in a single doctor's appointment. If your doctor is concerned that there might be something else causing your symptoms, you'll need further testing before migraine can be diagnosed. What are the steps of migraine diagnosis? The steps of migraine diagnosis will depend on your overall health, family history, and a few other factors. You can start by seeing a primary care doctor. In some cases, you might need to see a neurologist (a doctor who treats diseases and disorders of the nervous system) for further testing and treatment. During your migraine diagnosis, a doctor will: gather your medical history perform an exam order scans to rule out other conditions You can read more about each step below. Gathering your medical history Your doctor will need to gather a lot of information about your personal medical history and your family medical history to diagnose migraine. They'll ask you to provide as many details as you can about your symptoms. They'll also want to know about any other medical conditions you've been diagnosed with and about any other symptoms you've been having recently. You'll be asked about your diet, stress levels, activity levels, and other aspects of your lifestyle. Your doctor might ask you to keep a migraine journal until your next appointment. In the journal, you'll record every time you have pain and describe what that pain feels like. You can also record anything you do for the pain at home and whether it helps at all. For example, you might want to make note of whether certain over-the-counter (OTC) medications help. You'll need to provide as much family health history as you can. Since migraine tends to run in families, it's important for the doctor to know whether you have any relatives who've been diagnosed with migraine. It's also important to let them know about any other conditions that run in your family. Performing a medical exam During your exam, the doctor will do neurological tests to check your reflexes and see how you respond to sensations. They might also test your short-term memory. You'll have your blood pressure and pulse taken. A doctor will also check your head, shoulders, and neck. For many people, this is enough to diagnose migraine. Generally, you'll be diagnosed with migraine if you've had at least five headaches that have lasted between 4 and 72 hours and your headaches have at least two of these four characteristics: are located primarily on one side of the head cause pain that's pulsing or throbbing cause pain that's moderate to severe are made worse by normal physical activity Your headaches will also need to cause you nausea or sensitivity to light and sound to be categorized as migraine. A physical exam and thorough medical history allow a doctor to make the migraine diagnosis. However, in some cases, the doctor might not be certain that your symptoms aren't being caused by something else. In this case, you might need to move on to the next step. Ordering scans to rule out other conditions If your pain came on suddenly or if you're having other symptoms that aren't typically caused by migraine, your doctor might order more testing. This testing isn't for identifying migraine. It's for identifying other things that might be causing your pain, such as brain aneurysms or tumors. Testing might include: Magnetic resonance imaging (MRI). An MRI uses magnetic waves to create a detailed image of your brain. The MRI will look for infections tumors, bleeding, and other abnormalities in your brain that could be causing your head pain. Computed tomography (CT scan). A CT scan creates a detailed image of your brain. Just like an MRI, a CT scan can be used to look for medical problems that could be the source of your pain. Your doctor might also order blood work to help pinpoint other conditions that might be behind your pain and symptoms. Keep in mind that these tests are for identifying causes that aren't migraine. However, if no infections, tumors, or other possible causes are found, those causes can be ruled out. Ruling out other causes can allow your doctor to make a migraine diagnosis. Tips for finding a doctor to diagnose migraine Getting a migraine diagnosis is the first step to getting the treatment you need. Here are a few tips for finding a doctor: Start with your primary care doctor. Your primary care doctor might be able to diagnose migraine or refer you to a specialist who can. Check with your insurance. If you have insurance, you can use it to help find a doctor to diagnose migraine. Many insurance company websites even have an online tool that will let you search for a doctor to diagnose migraine who works with your insurance. Look online. Review doctors in your area who treat migraine. Consult organizations. Migraine organizations, such as the American Migraine Foundation, have resources to help find a doctor who treats migraine. What is migraine? It's common for people to think of migraine attacks as simply bad headaches, but that's not actually the case. Migraine is a neurological condition that causes severe pain. It can make it difficult to complete your daily activities or even get out of bed. Untreated, a migraine can last for several days. In addition to the pain, migraine episodes can cause nausea, vomiting, and other symptoms. Some people also experience warning symptoms before a migraine episode strikes. This is called an aura. An aura can cause a variety of sensory disruptions. However, not everyone with migraine experiences auras. Migraine can begin at any age but is most often diagnosed in people in their teens, twenties, or thirties. Migraine tends to run in families and is diagnosed more often in women than in men. The frequency of migraine attacks can vary from person to person. Some people might experience a few episodes a year, while others might have several in a single week. What are the symptoms of migraine? The symptoms of migraine can be very painful. Many people need to rest in a dark, quiet place during their migraine episodes to help manage their symptoms. Migraine symptoms often include: pain on one side of the head throbbing or pulsing pain sensitivity to lights sensitivity to sounds sensitivity to smells nausea and vomiting Some people also experience warning periods before a migraine. These warning periods have their own symptoms. The two warning periods are known as prodrome and aura. A prodrome normally occurs 1 or 2 days before a migraine. If you have a prodrome period, you might experience: mood changes irritability food cravings increased thirst neck pain or stiffness constipation An aura generally occurs right before a migraine. Some people also have aura symptoms during their migraine. Aura symptoms buildup gradually and can last as long as 1 hour. Symptoms include: vision loss visual hallucinations, such as flashes of light or bright spots seeing shapes difficulty speaking weakness on one side of the body tingling sensation on one side of the body uncontrollable jerks or tremors auditory hallucinations, such as sounds or music Some people experience further symptoms once a migraine episode has passed. This is known as post-drome and lasts for about a day. During post-drome, some people report feeling: drained confused exhausted elated or other mood changes a dull headache How is migraine treated? There are generally two parts to migraine treatment. The first part is stopping the pain and symptoms of migraine when they occur. The second is preventing migraine from occurring. Your treatment will include both of these parts. Treatments for stopping migraine symptoms include these medications: OTC pain relievers. OTC medications, such as Tylenol, Advil, and Excedrin, might help relieve mild migraine pain. They're often not enough to stop moderate or severe pain. Long-term use of these medications can also cause damage to your stomach lining. Triptans. Triptans are a class of medications that block pain pathways in your brain. They're available in pills, nasal sprays, or injections. For many people, they're an effective way to treat migraine. Dihydroergotamines. These medications are taken as nasal spray or injection. They're often useful for people whose migraine attacks last longer than 24 hours. In some people, they can cause migraine symptoms to worsen. Opioids. Opioids such as codeine can be effective in treating migraine. However, these medications are very strong and highly addictive. You'll generally only be prescribed opioids if no other treatment has worked to stop your migraine symptoms. Anti-nausea medications. People who have nausea and vomiting with migraine might benefit from taking anti-nausea medication along with a pain medication. Treatments for preventing migraine include: Identifying and avoiding triggers. You might be asked to keep a migraine journal to identify triggers that cause or worsen your migraine. Triggers can vary from person to person and might include weather, smells, hormonal changes, stress, certain foods, and more. Avoiding your migraine triggers can help prevent a migraine attack from occurring. Beta-blockers. Beta-blockers are often prescribed to people with high blood pressure, but they've been proven to be effective in treating migraine, as well. Your doctor might prescribe a daily beta-blocker to help prevent migraine, especially if you have frequent or severe attacks. Calcium channel blockers. Just like beta-blockers, calcium channel blockers are generally used for high blood pressure. They've been found to be effective at preventing migraine, especially in people who have an aura with their migraine. Antidepressants. Antidepressants can be used to prevent migraine. Some antidepressants can have unwanted side effects or interactions with other medications. Antiseizure medications. Some medications that prevent seizures can also prevent migraine attacks. Like antidepressants, these medications can cause unwanted side effects in some people. Botox injections. Botox is most often associated with cosmetic procedures, but it can actually be used in migraine prevention as well. You'll need an injection every 12 weeks or so if you go this route. It can take a while to figure out the right combination of treatments for you. Tell your doctor what's effective and what isn't. They can help you try other options until you find something that works. Can you prevent migraine? If you've already been diagnosed with migraine, your doctor can help you figure out the best prevention methods. Often, your first step will be keeping a migraine journal so that you can figure out what triggers your attacks and avoid them. Many migraine triggers are related to everyday health habits. This includes: not getting enough sleep not eating regular meals not exercising enough being under stress For some people, managing those things can help you prevent or lessen migraine. You can also avoid common trigger foods and drinks, such as: chocolate red wine cultured dairy foods with added MSG processed foods or smoked meats You can try eliminating these foods from your diet for a week and seeing whether you have fewer headaches. Some people are also helped by natural remedies that aren't medications.
Fast Company
7 days ago
- Health
- Fast Company
How AI brain mapping can improve disease detection
Traditional brain scans only show part of the picture. They can't fully capture how different regions of the brain communicate—an essential factor in detecting neurological diseases early. Dr. Rahul Biswas, a neurologist at the University of California–San Francisco, is working to change that with AI -powered tools that map these hidden neural connections. His groundbreaking research reveals how Alzheimer's disrupts brain communication in unexpected areas, challenging long-held assumptions about the disease. Now, through his company, Kaneva Consulting, Dr. Biswas is focused on transforming this science into practical diagnostic tools that can identify brain disorders long before symptoms emerge. Fast Company spoke with Biswas about how AI is revolutionizing brain health, from early disease detection to personalized treatments and everyday tech. The conversation has been edited for length and clarity. How are AI models revealing new insights about the brain that weren't possible with traditional neuroscience methods?
