Recent study links marijuana use to structural brain changes

 

 

Post  prepared by Amanda Baker, Drexel University College of Medicine Class of 2014

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A study recently published in the Journal of Neuroscience by Harvard researchers have linked casual marijuana use to structural changes in distinct areas of the brain.

These areas, the nucleus accumbens and amygdala, and are largely involved in recognition of reward, motivation, fear, and memory.  In this study, the brain scans of 20 young adult casual marijuana users were compared to those of 20 young adult non-users.

While the results clearly demonstrated significant structural differences between the two groups, the structural changes have not been correlated with consequences in mental or physical functioning.  In other words, researchers aren’t entirely sure of the impact of these brain changes.

 

Casual marijuana use may damage your brain

The debate regarding the use of marijuana medically and recreationally is ongoing in the United States.

Although the Drug Enforcement Administration(DEA) categorizes this drug as Schedule I, “with currently no accepted medical use and a high potential for abuse”, many argue that there is, in fact, much benefit to medical marijuana, especially in comparison to other sedating pain medications.

This is reflected in 21 state laws which have legalized medical marijuana to varying degrees.

Last summer, Dr. Sanjay Gupta completed a documentary “Weed” highlighting the benefit of medical marijuana:

However, some states such as Washington and Colorado, have gone one step further by legalizing marijuana for both recreational and medical use.

Given the ongoing research on the effects of marijuana, perhaps this new study will call into question continued legalization of the most widely used recreational drug in America.

 

Click here to find out more.

 

Memory misplaced

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Post written by Dr. Farida A. Malik , PGY3 Medical Resident, Monmouth Medical Center

Case Summary

This 69 year old lady had a remote history of breast cancer, hypertension and hypothyroidism.  She was brought to the Emergency Room by her husband because of abrupt onset confusion after waking up that morning. She was disoriented and was noted to ask the same questions over and over again. She had no difficulty walking, talking or dressing herself. She denied having headache or visual problems. There was no history of head trauma, seizures or any prior similar episodes.

When she was seen in the in the ER she knew her name and recognized her husband.  She was able to follow simple commands.  She had no recollection of events since morning or the day before. She repeatedly asked how she got to the hospital, despite being told several times that her husband brought her. Neurological examination otherwise was unremarkable.

CT scan of head, MRI of the brain and EEG were all normal.

She was diagnosed with TRANSIENT GLOBAL AMNESIA.

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The family was reassured about the benign nature of the condition and she was discharged home the next day still with memory lag.

Discussion

Transient global amnesia (TGA) is a clinical syndrome of reversible anterograde amnesia accompanied by repetitive questioning that occurs in middle-aged and elderly individuals.

The incidence of TGA is 5.2 to 10 per 100,000 per year overall, but 23.5 to 32 per 100,000 per year in adults aged 50 and over.

During a TGA episode recall of recent events simply vanishes. One may also draw a blank when asked to remember things that happened a day, a month or even a year ago.  Unlike “soap opera amnesia” (Jason Bourne) affected patients do remember who they are and recognize the people they know well.  But that doesn’t make their memory loss less any less disturbing.

Fortunately, episodes are usually short-lived, recover spontaneously, and are unlikely to recur.

The precise cause of TGA is unknown.  Atherosclerotic risk factors (eg. hypertension, diabetes, hypercholesterolemia) are not associated with TGA.
However there may be a link between TGA and history of migraines.

The primary site of neurologic functional disturbance is the medial temporal lobe and hippocampus.
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The pathogenesis of this transient disruption is unknown. Current theories include arterial ischemia, venous congestion, and migraine, but no theory explains all of the clinical features.

The diagnosis is made by the following signs and symptoms:

  • Sudden onset of memory loss, verified by a witness
  • Retention of personal identity despite memory loss
  • Normal cognition, such as the ability to recognize and name familiar objects and follow simple directions
  • Absence of signs indicating damage to a particular area of the brain, such as limb paralysis, involuntary movement or impaired word recognition
  • Duration of no more than 24 hours
  • Gradual return of memory
  • No evidence of seizures during the period of amnesia
  • No history of active epilepsy or recent head injury

Some common triggers identified are:

  • Sudden immersion in cold or hot water
  • Strenuous physical activity
  • Sexual intercourse
  • Medical procedures, such as angiography or endoscopy
  • Mild head trauma
  • Acute emotional distress, as might be provoked by bad news, conflict or overwork

There are no confirmatory diagnostic tests. The initial evaluation and management of patients with TGA focuses on excluding other diagnoses and should include the following:

  • If the patient is symptomatic on presentation, the patient should be observed in the hospital until the amnesia resolves.
  • Diagnostic testing includes oxygenation status, serum electrolytes, glucose, and a toxicology screen.

The need for further testing varies depending on the circumstances, such as how typical the event is for TGA, the presence of vascular risk factors, and whether the ictus was observed. Patients with recurrent or brief episodes, or activity suggesting motor automatism should be evaluated with EEG for possible epilepsy. A neuroimaging study may be performed in all patients, preferably a brain MRI with DWI, to exclude acute ischemia, head trauma, and other causes.

Treatment is not required for TGA. The condition usually does not recur, and the patient does not need to be restricted from driving unless events are recurrent.

There is no increased risk of mortality, epilepsy, or stroke following TGA as compared with age-matched controls.

Acute Back Pain, What Not To Do!

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70-80% adults have experienced acute back pain, almost 30% seek medical attention, and this problem is one of the commonest reasons for a doctors’ office visit.

Most cases are caused by sprains or tears in one of the numerous muscles or ligaments in the back triggered by twisting or lifting something heavy.

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These “soft tissue” injuries will usually improve on their own within a few weeks with anti-inflammatory medications and physical therapy.

However a recent study showed that more and more such patients are getting unnecessary imaging studies right away leading to surgeries and other invasive procedures that they don’t need.

Possible reasons cited for the necessary procedures include patient expectations and financial incentives for doctors.

flag_status_redDoctors shouldn’t immediately order an MRI or CT scan to determine the cause of back pain if a patient doesn’t have any red flags such as tingling in the legs — a sign of a nerve problem such as spinal stenosis — or a previous history of cancer.

Otherwise, imaging studies ordered for nonspecific back pain may reveal incidental disk problems, the result of aging, and not the cause of the symptoms.

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This will then often lead to unnecessary and unproven interventional pain management procedures.

Most back pain patients simply need to be told that their pain will improve with antiinflammatory medications, physical therapy, massage therapy, and/or supervised exercise programs.

However, in the words of Dr. John Mafi, one of the study’s authors, “it takes longer to sit and reassure patients that their pain will likely resolve on its own than it does to order an MRI.”

Correct clinical diagnosis of dizziness in the ER could save $$ billions

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We have already blogged about the danger of escalating health costs in the USA.

The cost of emergency room visits for severe dizziness has grown exponentially in recent years, topping $3.9 billion in 2011 and projected to reach $4.4 billion by 2015.

Investigators from Johns Hopkins estimate that half a billion a year could be saved immediately if emergency room physicians stopped the routine and excessive use of head CT scans to search for stroke in dizzy patients, and instead used simple bedside physical exams to identify the small group of patients that truly needs imaging.

Click here to find out more about the Johns Hopkins study.

Click here to find out more about the hidden dangers of unnecessary CT scans.

Once they understand how inner ear disease can cause vertigo and nystagmus, any physician can use our simple clinical scheme to distinguish inner ear problems from more serious and rarer central causes like stroke in dizzy patients.  Click here to find out how.

A ripping yarn – a tale of cervical artery dissection

Case Summary:
This 46-year-old woman was healthy except for a history of occasional migraine headaches and cigarette smoking. On the day of admission she had fallen down a short flight of steps carrying a heavy box. About 2 hrs later she complained of some neck pain.  Then later that evening developed abrupt onset left sided weakness. She arrived at the emergency room within 1.5 hrs of the onset of weakness. On examination, she was alert, but she had a right gaze deviation (she wouldn’t look to the left side) and the left side was completely paralyzed. She had a normal brain CT scan.

The stroke team was notified, and she was given intravenous thrombolytic (“clot busting”) drug therapy within 1/2 hr of her arrival at the hospital and 2 hrs since the onset of her symptoms.

Carotid ultrasound subsequently showed no flow in the right internal carotid artery, and carotid arteriography subsequently showed near occlusion of the artery from an arterial dissection (see image below, red arrow):

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What is cervical artery dissection?

Cervical artery dissection is caused by bleeding inside the wall one of the major arteries in the neck.

This process is thought to be triggered by local injury to the inside layer of the vessel wall.

Cervical artery dissections occur from blunt trauma:

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Cervical artery dissection can also occur after minor trauma, particularly in someone with a genetic predisposition:

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What diseases predispose to arterial dissection?

There are some specific syndromes such as Marfan syndrome, Pseudoxanthoma elasticum and Ehlers- Danlos syndrome type IV that are associated with a weakness in the arterial wall making an arterial dissection more likely:

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In other cases, the specific cause of arterial weakness is unknown, but there is ongoing research to try to identify genetic links.

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What happens after a cervical artery dissection?

Symptoms can be caused from the damaged arterial wall itself (local symptoms) and some affected patients will later develop strokes.

Local symptoms include neck pain, unusual headache and/or Horner’s syndrome.

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L Horner’s syndrome (small pupil and drooping eyelid) caused by damage to the sympathetic nerve fibers in the arterial wall from carotid dissection. Click here to find out more about Horner’s syndrome and other causes of unequal pupils.

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What about stroke?

Stroke symptoms only occur in 25-30% dissections and can occur several days after the neck trauma and/or onset of local symptoms.

The arterial dissection narrows the space inside the blood vessel (the lumen), so less blood flow gets to the brain:

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A carotid artery dissection with blood clot inside the arterial wall (left) leading to narrowing of the vessel lumen and less blood flow (right).

Cervical arterial dissections can also cause stroke when pieces of blood clot break off and move with the blood flow only to block small arteries further inside the brain (cerebral thromboembolism), or if the dissection tracks across (and blocks off) an arterial branch (see below):

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How is arterial dissection diagnosed?

Magnetic resonance imaging is probably the easiest way to make the diagnosis:

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MR angiogram (left) showing tapered occlusion of the left internal carotid (white arrow) from dissection. Fat suppressed T1 weighted MR axial image through the dissected cervical artery (right) showing bright blood within it’s wall (black arrow) from dissection.

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How is it treated?

In most cases the arterial dissection ultimately heals on its own without any surgical intervention.  There has been some controversy surrounding the use of anticoagulant vs anti-platelet drugs for stroke prevention after cervical artery dissection, but most current data favors the use of the anti-platelet drug aspirin:

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Of course, for patients presenting with symptoms of acute stroke, throbolytic therapy is also an option, and can improve outcome without increased risk in stroke from dissection:

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Click here to find out more about cervical artery and dissection and stroke.

Click here to find out what to do if you think your having a stroke.

Click here to find out more the certified stroke center at Monmouth Medical Center.

Shouldn’t I have a brain MRI, doctor?

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Migraine is extremely common, with a lifetime incidence of 43% in women and 18% in men, and a median age of onset of 24-5.

The vast majority of headache patients have migraine and need a careful history & physical examination, followed by appropriate treatment, not a brain imaging study.

Studies have shown that a brain imaging study will disclose an “abnormality” in about 1% of unselected headache patients, similar (if not less) than asymptomatic test subjects.

Furthermore, there are potential complications involved with brain imaging:  Some patients are claustrophobic and require sedation, even a general anesthetic.  Many “abnormalities” are innocuous, unrelated to the headache and do not require treatment.  However, these headache patients with such  “incidentalomas”  are left with the conclusion that there is something wrong with them, and may be subjected to further unnecessary follow-up studies.  A few end  up getting unnecessary invasive tests, which actually hurt them.

However, not a day goes past without a migraine patient asking me for a brain imaging study, or for that matter a patient referred to the office worried about an “incidentaloma” identified on a brain imaging study which should never have been done in the first place.

That’s not to say brain imaging is always unnecessary in every headache patient.

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Carefully selected patients with the following “red flag” characteristics might still need a scan:

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This approach is supported by the American Academy of Neurology, whose position is that neuroimaging usually is not warranted for patients with migraine and normal neurologic examination, only for patients with atypical headache features.

Find out more about migraine and headache here.

Epilepsy surgery and functional MRI

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Epilepsy surgery is an option for patients with intractable partial onset seizures that are not controlled by oral medications.  Epilepsy monitoring is used to localize the seizure focus, often a lesion or abnormal area of brain located in the temporal lobe.  That part of the brain is then carefully removed to prevent future seizures:

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A patient with a brain abnormality in the R temporal lobe (top) undergoes brain surgery to remove that area of brain and prevent future seizures.

Epilepsy surgery is very effective and yet still underutilized for treating seizures.

Left temporal lobe resections are more risky that right-sided cases, because the left hemisphere controls language functions in most (even left handed) patients.  Surgeons have to be very careful planning seizure surgery on the left side to be sure that they do not damage brain critical for speech and language and leave the patient with aphasia.

That’s where functional magnetic resonance imaging (fMRI) comes in.  fMRI goes beyond the conventional imaging of brain structure, and can actually localize regional brain functions by detecting changes in regional blood flow in response actual or imagined activity.

fMRI is increasingly being used to evaluate candidates for epilepsy surgery by identifying important functional regions within the brain, including unpredictable patterns of functional reorganization, to prevent unexpected post-operative deficits.  Click here for a link to a paper with illustrative cases.

Monmouth’s New Onset Seizure Center Opens in June!

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New onset seizures can be isolated events or the harbinger of future epilepsy.

Decisions about starting medications and restricting driving are complicated, and are best made by neurology sub-specialists (“epileptologists“) after a detailed evaluation that usually includes an electroencephalogram (EEG) and brain magnetic imaging study (MRI).

Monmouth Neuroscience Institute is pleased to announce the opening of the region’s first New Onset Seizure Center in June 2013.

Patients who come to the emergency room with their first seizure can be stabilized and then sent home with instructions to follow-up in New Onset Seizure Center, an integral part our Certified Epilepsy Center within one week.

All patients coming to the center they will undergo an EEG, MRI of the brain and a visit with one of our board certified fellowship-trained epilepsy experts during a single visit.

This avoids hospitalization and hasty decisions about medical management.

Click here to find out more about the center.

Back pain? Could it be coming from inside your head?

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Most people agree that emotional stress or psychological factors can make any pain, including back pain pain worse.

However, the concept of “stress-related” or psychosomatic back pain, which is primarily caused by psychological and emotional factors, is usually harder to grasp.

It is important to make affected patients understand that even though psychological factors may be causing the physical symptoms, the symptoms are not imaginary

Instead, the unresolved emotional tension is pushed out of awareness into the unconscious mind, which then causes changes in the body’s nervous system, leading to muscle tension, spasm and the back pain experienced by the patient.  This chronic pain can lead to insomnia, fatigue, disability and then depression in a viscous feedback cycle:

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This syndrome can be hard to recognize for 2 reasons:

First, the pain may actually start with an identifiable incident that caused lower back sprain or strain, but then continue as the result of emotional factors long after any physical  injury should have  healed.

disc bulge

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Second, MR imaging studies are so sensitive, that when used inappropriately they may demonstrate incidental “findings” such as a “disc bulge” or “degenerative disc disease”, and the pain becomes attributed to this even when stress is the actual culprit.

The end result is that the affected patient gets sent for endless cycles of physical therapy, then epidural injections and even surgery.  Despite these measures, many patients continue in chronic pain.

If the back pain can be correctly identified as stress related in the first place, then the patient can be encouraged to “think psychological, not physical”,  and get some psychotherapy to address the unconscious issues.

Obviously, this approach is very different than the way most physicians manage patients with back pain.

Perhaps it’s time for a game change?

Click here to find out more.

New Brain Imaging for Alzheimer’s Disease

Amyloid proteins in normal brains (left) and abnormal ones (right) visualized with GE Healthcare’s PET tracer flutemetamol.

Alzheimer’s disease is the commonest cause of dementia, and as the population is aging, it’s prevalence is increasing.

Alzheimer’s disease presently affects 5 million Americans aged 65 or older.  Without a major medical breakthrough, by 2025 this number is expected to have risen to 7 million, and by 2050 it could reach 14 million

The costs of caring for Alzheimer’s patients is also increasing, estimated at $203 billion in 2013, and $1.2 trillion by 2050,  including a 500% increase in combined Medicare and Medicaid spending.

Clearly, finding that major therapeutic breakthrough is crucial, and had been identified as a priority by the Obama Administration.

The first barrier to starting any clinical trial is accurate case ascertainment – we have to be able to correctly identify early Alzheimer’s patients for new experimental treatments.

So far, the only definitive test for Alzheimer’s disease is examination of brain tissue (usually obtained at autopsy) for identification of the characteristic pathologic changes of Amyloid paque and Neurofibrillary tangles:

Alzheimer’s disease is usually diagnosed based on  clinical criteria, but many patients diagnosed this way are later found to have other causes of dementia when their brains are examined at autopsy, in other words they were misdiagnosed as Alzheimer’s.

With more research trials and potential new effective therapies on the horizon, it is going to become more important to establish a diagnosis of Alzheimer’s more accurately and earlier, perhaps even pre-symptomatically (i.e. mild cognitive impairment or MCI), so that treatment to reverse the build up of plaque and tangles is more likely to be effective.

New positron emission tomography (PET) technology can actually quantify the amount of amyloid in affected patients’ brains.  A recently published small study showed a very high correlation between amyloid identified on PET scans and amyloid plaque demonstrated in brain biopsy specimens taken from demented patients.

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These tests are going to be very important for research studies.

However, don’t rush to your private doctor’s office asking to have one done just yet!

Although approved by the FDA, these test are not yet covered by Medicare or other insurance covering, and cost between $1500 and $3000.

Furthermore, these are new tests, and their role in clinical neurology practice in still unclear.

Some of these issues were recently clarified in a report by the Amyloid Imaging Taskforce convened by the Alzheimer’s Association and the Society of Nuclear Medicine and Molecular Imaging:

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This taskforce concluded that a Amyloid PET scan is indicated for:

Progressive memory impairment or dementia with atypical features, where a positive PET would indicate definite Alzheimer’s, and a negative scan would rule it out and lead to further testing for other possible causes.

Younger patients (aged 50-65) with suspected Alzheimer’s, in whom making a definitive diagnosis is crucial for log term planning and future medical decision making.

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The taskforce concluded that a Amyloid PET scan is unnecessary and/or unhelpful for:

Patients with typical Alzheimer’s disease,

Determining the severity of dementia,

Asymptomatic patients with a family history of dementia or positive apolipoprotein E4 status,

Patients who complain of memory loss but have no objective findings,

Testing purely for medico-legal, disability, insurance or employment related issues.

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Find out more:

Click here to find out more about Memory loss, Mild Cognitive Impairment and Alzheimer’s.

Click here to find out more about diagnosing Alzheimer’s.

Links to the Alzheimer’s Association, Alzheimer’s Foundation of America and CDC Healthy Brain Initiative