Today I had a lovely Sunday brunch with an old friend of mine. At some point, the famous frozen salmon study became the topic of our discussion (if you haven’t heard of it before, you can read about it by clicking this link: http://www.wired.com/2009/09/fmrisalmon/). Our discussion is actually irrelevant to this post. Two hours later, the brunch ended and I drove home. As I turned into my driveway, I saw the same cat I always see on my street. I usually dismiss its existence (pun intended). This time was different. It made me think about Schrödinger’s paradox (if you would like to know more, I highly recommend the book, In Search of Schrödinger’s Cat: Quantum Physics and Reality). As a person who has been interested in quantum theory since the age of 6, I have a tendency to rationalize everything from a cosmic perspective. So now the question becomes…what if the salmon wasn’t dead after all?
“We are what we repeatedly do,” Aristotle once proclaimed. Now that we have welcomed the New Year, it is the perfect time to rewire our brains to develop better habits and reverse our old ones. Every year, millions of people make New Year resolutions with the promise that this year, they will stick to them. So why is it that so many people fail to live up to their promises? The answer lies within our own habits. By acknowledging the impact that our habits have on our everyday lives, we can increase the chances of reaching our goals. Over the past few years, research on habit formation has been a hot topic, especially in the field of neuroscience. Simply stated, habits are behaviors that are automatically performed. For example, having a soda for lunch everyday, procrastinating at work or school, and tardiness are all habits, albeit negative ones. Some positive habits you may have are reading the newspaper, brushing your teeth, and exercising, just to name a few.
There is no doubt that habits are intricately complex and difficult to flesh out, especially because each individual habit has distinct neurological underpinnings. It is plausible that nicotine addiction is similar to a binge-eating habit in terms of neurobiology. On the other hand, it would be erroneous to posit that the neurological mechanism involved in a cigarette smoker’s addiction is the same as the mechanism involved in another person’s compulsive nail biting habit. Understanding how habits are formed and how they can be reversed not only has implications for healthy individuals, but also for clinical populations. For example, patients who are diagnosed with obsessive-compulsive disorder (OCD) are essentially suffering from an inability to break their habits. Research findings reveal abnormality in anterior cingulate cortex and insula function in individuals with hoarding disorder (HD), a subtype of OCD. Furthermore, it has been found that individuals with HD have difficulty with decision-making, a process modulated by the lateral habenula in healthy individuals. It goes without saying that our habits effortlessly guide our behavior for better or for worse. When we’re faced with a specific situation, it’s simply more efficient for us to rely on prefixed schemas, a primary reason why habits are so difficult to break. When our negative habits have ramifications, a less automatic and perhaps more cognitively taxing approach must be taken. For example, you may have a habit of checking your phone while you’re driving. You know about the risks, but for whatever reason still choose to reach for your phone while driving. The crux of the problem is that you’re in a schema where you have performed this particular act countless times in the past. The control our habits have over our decision-making process is overwhelming. A possible solution to this issue would be to leave your phone in the trunk of your car. This should be fairly easy to do, especially knowing that your habit is putting your own and others’ lives at risk. You will be surprised to see that this new habit will become automatic after an average of 21 days. After your old habit is overridden, you can keep your phone in the car with you, but you must be cautious. It is recommended that you avoid any precipitating factors that may trigger your old habit (e.g. keep your phone on silent).
Let’s examine this simple, seemingly harmless habit of checking messages on your smart phone in bed before falling asleep every night. There is substantial evidence indicating that the quality of sleep is significantly diminished by the use of cell phones before bedtime. Looking at a self-luminous screen stimulates the human circadian rhythm and suppresses levels of melatonin, a hormone that regulates sleep. The electromagnetic radiation that is emitted from these devices raises concerns as well. Research has established links between sleeping with a cell phone nearby and depression, personality changes, and mood swings. The areas of the brain influenced by this habit, structurally and functionally, have also been found to deteriorate our attention system. Taken together, these risks pose a serious threat to our well-being. Can you think of a potential solution to breaking this habit?
As difficult as it may seem to improve our habits, neuroplasticity has made it possible for us to accomplish any cognitive feat within the constraints of our own capacity. Without neuroplasticity, traumatic brain injury (TBI) patients wouldn’t be able to walk, talk, or eat again. Similarly, we wouldn’t be able to teach ourselves previously unknown skills, such as mental arithmetic. It is important to note that neuroplasticity also has its own limits, depending on factors such as degree and location of injury in the brain. There are TBI patients with extensive cerebral contusions who never learn to walk or talk again. Nonetheless, neuroplasticity is usually evidenced in the period of spontaneous recovery post-injury in majority of clinical cases, including the profound ones. In addition to the cortical remapping that occurs in response to injury, neuroplasticity also applies to neuronal changes resulting from learning. Learning a second language is one example of this. Research has shown that after the age of 12, learning a second language is exponentially more difficult, a finding in concordance with neuroplasticity research.
The correlation between habits and anatomical changes in the brain is an interesting one. Scientific research lends empirical support to the hypothesis that habits can directly alter our neurobiology. For example, research has shown that consuming snacks with high caloric content decreases serotonin transporters in the human hypothalamic region. Another example is that physical exercise habits correlate with gray matter volume of the hippocampus in healthy individuals. Needless to say, habits are highly constrained and must be examined independent of each other. The exact nature of the relationship, whether we are genetically predisposed to develop certain habits, or habits facilitate neuroanatomical changes, remains elusive.
Over the last few years, I devoted a lot of my free time to reading. Here, I have compiled a list of my all-time favorite books. It wasn’t easy to pick twenty out of the myriad readings I completed throughout high school, college, and graduate school. The list below includes fiction and non-fiction books that I have read and found to be thought-provoking, educational, and inspirational. These are books that I believe everyone should read at some point in their lifetime, regardless of their age, gender, or profession. Our brains have a limitless capacity to learn new information, so expanding our literary horizons is beneficial. My top twenty books, in no specific order, are:
3. The Politics of Truth – Michel Foucault
4. The Tipping Point – Malcolm Gladwell
5. Syntactic Structures – Noam Chomsky
6. Into the Wild – John Krakauer
Verbal & nonverbal communication work together. Use body language that supports your words to reinforce the message.
The words “actually” and “I think” limit your authority and conviction. Don’t use them. Instead, be declarative.
When you are under pressure, remain objective. Pause and take a long, deep breath before you speak.
Speak with adequate pauses. This gives a sense of authority and confidence in what is being said.
Use cadence to make your speech more poignant. Cadence imparts a harmonious effect to any speech.
Pace yourself. Speaking too fast tells your audience you are nervous, so take a deep breath and be mindful of your rate.
Say only words! Avoid fillers such as “um, uh, er, aaah,” and sounds that only masquerade as words, such as “like.”
Monitor your volume and tone. They give a snapshot of your feelings. Keep your tone even and calm. It communicates confidence and respect.
Don’t wing it! Know what you want to say and how you want to say it— preparation is key for a successful presentation.
When dealing with a sensitive topic, be clear, concise, correct, and kind. This is important for email also.
When leaving a voice mail, sound positive, polished and professional. People will get a wonderful first vocal impression!
Dress the part! When you look great, you feel more confident & comfortable— and that will come across to your audience.
Keep this in mind— your audience is there because they want to hear what you have to say. They are rooting for you!
When it comes to audiological testing, everyone is a little more than anxious. You might say to yourself, “I’m a speech therapist, I evaluate and treat disorders of speech and language, not hearing.” While this statement has some merit (granted our caseload has more clients than hours in the day), as experts in communication disorders, it is essential for us to know not only basic audiological screening techniques, but also the tangential procedures that allow us to conduct a comprehensive evaluation. It is important to be cognizant about the role that auditory impairments play in disorders of speech and language, so that we can have a thorough understanding of the etiology.
If you’ve taken an audiology course in graduate school, surely you’ve heard about the masking procedure. Simply stated, masking is a procedure we use while acoustically testing two ears, separately. The process is very much like when you get an eye exam, and you don’t want to test both eyes at the same time. You separate them by covering one then testing the other to determine if it is normal or impaired. Similary, noise is used as a masker during an audiological evaluation, hence the term masking. Noise is introduced to one ear while the other ear is tested with a tone (or speech signal). To indicate that the hearing thresholds were obtained using masking, masked threshold symbols are used on the audiogram.
Here, I will explain the masking procedure in detail. Implications for when to mask, how to mask, and how much to mask will also be discussed.
Interaural Attenuation: The reduction of sound between two ears (from TE to NTE) when presented via air or bone conduction. This is the number of decibels (dB) lost in cross-over.
Shadow Audiogram: When the thresholds of the left ear mimic the bone conduction thresholds of the right ear. This is a tell-tale sign of cross-over.
Occlusion Effect: The enhancement of low frequency bone conduction thresholds when the outer ear is occluded.
When to Mask
A/C: if there is a difference between the 2 ears of 40 dB or greater, you need to mask.
B/C: if there is an air-bone gap greater than 10 dB you need to mask.
SRT: SRTte > SRTnte by 45 dB or SRTte > BCnte in speech range by 45 dB or more.
SRS: PLte > SRTnte by 35 dB or PLte > BCnte in speech range by 35 dB or more.
How Much to Mask
Undermasking: Not enough masking in the non-test ear to mask the test stimulus.
Overmasking: Excessive level of masking crosses over and elevates thresholds.
Effective Masking: Minimum amount of noise required to just mask out the signal keeps signal from crossing-over to non-test ear.
AC: ACnte + SF = M
BC: ACnte + SF + OE = M
SRT: (PLte – 35 dB) + PTAnte
WDS: (PLte – 25 dB) + PTAnte
SF = 10 dB
OE = 20 dB @ 250 Hz, 15 dB @ 500 Hz, 5 dB @ 1000 Hz
Remember 35 dB for SRT, 25 dB for WDS
A/C: An earphone is placed over the test ear and masking is applied to the non-test ear through another earphone.
B/C: With mastoid placement, the bone conductor is placed on the mastoid of the test ear and masking is applied to the non-test ear through an earphone, which is placed in front of the pinna of the non-test ear.
Hood Plateau Method: 3 consecutive positives or 3 consecutive 5 dB masking level increases at the same pure tone intensity level. Width of plateau is affected by the amount of interaural attenuation, the A/C threshold of the non-test ear, and the B/C threshold of the test ear.
Central Masking: A threshold shift in the test ear resulting from the introduction of a masking signal into the non-test ear that is not due to cross-over. Average is 5 dB.
Masking Dilemma: Ineffective masking level achieved due to bilateral moderate conductive hearing loss.
What do we do when there’s a masking dilemma, you ask?
But consider using the Weber Test (with asymmetrical conductive hearing loss).
Use insert earphones (insert earphones increase the interaural attenuation levels from an average of 55-65 dB to an average of 80 dB).
Also, know the immittance measures, which validate behavioral audiometric results.
Impedance: reflected energy
Admittance: absorbed energy
Immittance: measured through absorbed and reflected energy
Air pump: +/- pressure
Microphone: input (analysis system)
Loudspeaker: output (probe system)
Probe tip with cuff (hermetic seal). Goes into ear canal and delivers pressure and signal
Measurements of Immittance Measures
Static Compliance: measurement of the mobility of the tympanic membrane
Tympanometry: measurement of the pressure-compliance of the tympanic membrane
Type A: represents normal middle ear function. Peak occurs between 50 to -100.
Type C: retracted TM. Static compliance is within normal limits but peak is off. More negative than -200. Can indicate beginning or resolution of Otitis media; beginning of Eustachian tube malfunction.
Type As: Very shallow. Represents abnormal stiffness. Compliance measures are abnormally low. Could be due to scarring on the TM or the beginning stages of Otitis media.
Type Ad: Represents excessively flaccid. Peak is abnormally high – appears as if it doesn’t come together at the top. Could be due to scarring on the TM or disarticulation of the ossicles.
Type B: Flat. Represents restricted mobility, a great deal of reflection is occurring. Compliance measures are abnormally low. Could be due to active Otitis media or significant fixation of the ossicles.
C1= volume of ear canal from the tip of probe all the way to tm
C2= how much mobility how much compliance you have with the TM
TM Perforation: C1 value will be very high. Air is going right through to the Eustachian tube.
Effusion: Value of C1 has to be > .27
Canal Wall: if the probe is up against the canal wall C1 will read 0 or .1
Types of Units
Relative: data on a set scale of 0-10
Absolute: data in exact units of measure (daPA)
C1 – C2 = SC/SA (C1 = ear canal volume, C2 = measurement at peak)
Normal = 0.3 – 1.4 mmho/cc3/m
Limited/Restricted = < 0.3 mmho/cc3/m
Excessive/High = > 1.4 mmho/cc3/m
Acoustic Reflexes: stapedial reflex of middle ear muscle contracting and causing a change in TM position. A good way to confirm behavioral results.
Ipsilateral AR Pathway
Inner Ear (cochlea)
Auditory Nerve (CN VIII)
Cochlear Nucleus (ventral)
Superior Olivary Complex (medial)
Contralateral AR Pathway
Superior Olivary Complex
Present vs. Absent AR
Acoustic reflex occurs: 70 – 90 dB (normal). Absent = hearing loss (< 50 dB = hearing loss with recruitment)
Absent acoustic reflex due to: hearing loss (severe to moderate), neurological involvement, middle ear pathology
Eustachian Tube Function: Valsalva maneuver (pinch and blow), Toynbe maneuver (pinch and swallow).
Reflex decay: Hold signal for 10 seconds. Normal will show reflex for 10 seconds, pathologic system will not.
Electrocochleography: Monitors the function of the inner ear. Often used prior to cochlear implantation to make sure auditory nerve is intact. It’s also to screen for Meniere’s Disease. You’ll need a sound delivery tube, electrode wire, foam ear plug, and electrode tip.
Auditory Brainstem Evoked Responses: Assess the function of the auditory pathway up to and including the brainstem.
Middle Latency Auditory EP: Relating responses to generators. Middle latency responses are at VI (medial geniculate in the thalamus) and VII (auditory radiations, thalamo-cortical).
Late Cortical Auditory EP: At the cortex
Otoacoustic Emissions are acoustic energy produced by the healthy cochlea and recorded in the external auditory canal. These are acoustic signals, not electrical potentials.
Evoked: from stimulating the cochlea – getting pre-neural activity. This is an efferent response.
Non-evoked: spontaneous. Nothing stimulates it. The ear acts as a sound generator – 20 dB SPL. Found in 60% of normal ears. Females tend to have stronger spontaneous OAEs. Right ears tend to have stronger spontaneous OAEs. Usually measurable in the 1K-2K Hz range. The same person can have multiple emissions.
Distortion Product (DP OAEs)
Tonal responses located at precise frequencies determined by 2 simultaneously presented pure tones. Choose which part of the cochlea you want to stimulate.
Two discrete pure tone frequencies, F1 and F2 are introduced into EAM.
Each tone has specific amplitude L1 or L2 (50-75 dB SPL).
Input frequencies are related by a pre-determined ratio called a “fratio” (1:1 – 1:3). If F1 = 1K Hz, then F2 = 1.1 – 1.3K Hz.
With a transient signal (click, gated tone pip). Children have more robust TEOAEs. Amplitude decreases with age. There is a correlation between stimuli and response amplitude: intense signal yields intense response to a point.
Most clinicians know that doing a motor speech evaluation is an overwhelmingly tedious task, especially when you only have 1-2 hours to complete the assessment. I have compiled a list of factors that should be evaluated to arrive at an accurate diagnosis.
1. Case History: Primary and secondary medical diagnosis, site of lesion in CNS (MRI, CT scans), and date of onset/course of problem. Ideally, the patient provides information putting on display the salient features and severity of the problem.
2. Patient Interview: Basic data, family/home situation, description including onset, perception of speech, how it feels to speak, changes in appearance, associated deficits, swallowing difficulty, physical/mobility status, and earlier instances of nervous system damage.
3. Cognitive / Communication Assessment: Orientation, comprehension of two-step directions, and expressive language.
4. Respiration: Subglottic air pressure for phonation (damage can cause decreased air, short phrases, and breathy vocal quality).
5. Phonation: Vocal fold vibration dependent on complete adduction of folds and sufficient subglottic air pressure to cause folds to vibrate (damage can cause hypotonicity or hypertonicity).
6.Resonance: Provides proper tonality for oral and nasal phonemes, dependent on functional raising and lowering of velum (damage can cause weakness or slowness – incomplete velopharyngeal closure resulting in hypernasality).
7. Articulation: Requires appropriate timing, direction, force, speed and placement of oral structures (damage to nerves most commonly results in imprecise consonants).
8. Prosody: Melody of speech (damage can effect pitch, loudness, prolonged intervals between syllables or words).
9. Oral Mechanism Exam (OME): Tone, strength, and range of motion of oral motor musculature.
7. Alternating Motion Rate (AMR): Assess speed (slow/fast), dysrhythmia, uneven loudness, uneven pitch, tremor, duration between syllables, blurring between syllables, hypernasality, nasal emission, restricted amplitude of lips or jaw, imprecise/distorted consonants (average /p/ and /t/ – 5-7 reps per second or 30-35 reps in 5 seconds, /k/ is slightly slower).
9. Sequential Motion Rate (SMR): More difficult than AMR; average is 5 per second. Useful in diagnosing apraxia. With apraxia, patient may exhibit delay in starting, may exhibit phoneme substitutions, incorrect sequencing of syllables, and groping for correct placement.
10. Stress Testing: Screen for Myasthenia Gravis – a disorder that causes rapid fatigue of muscles during sustained motor tasks (patient counts quickly from 1-100; assess for rapid deterioration in articulation, resonance, or phonation).
11. Test for nonverbal oral apraxia: If there is evidence of groping or inability to sequence oral movements, test for apraxia. May observe groping behaviors, hesitations during non-speech oral movements, disrupted sequence of oral movements that are not verbal, can have nonverbal oral apraxia without apraxia of speech and apraxia of speech without nonverbal oral apraxia.
12. Test for apraxia of speech: Inability to sequence voluntary movements for speech. May demonstrate hesitations, revisions, omissions, inconsistent errors in articulation, automatic and emotional speech are usually intact, as are complete automatized sequences such as counting, days of week. Family will usually be surprised that clear utterances occur during emotional situations. To assess, have patient repeat words. If unable to repeat, present in written form. The goal is to increase complexity. List should also contains low frequency words. If patient has apraxia of speech, he/she will observe many sequencing/articulation errors. Next set of single syllable words begin/end in same phoneme should be easier to produce; however, if patient has difficulty it will give you an indication of the severity of apraxia.
13. Functional Communication Measure: Level 0 – unable to test, Level 1 – production of speech is unintelligible, Level 2 – spontaneous production of speech is limited in intelligibility; some automatic speech and imitative words or consonants/vowel (CV) combinations may be intelligible, Level 3 – spontaneous production of speech consists primarily of automatic words or phrases w/ inconsistent intelligibility, Level 4 – spontaneous production of speech is intelligible at the phrase level in familiar contexts: out of context speech is generally unintelligible unless self cueing and self-monitoring strategies are applied, Level 5 – spontaneous production of speech is intelligible for meeting daily living needs; out of context speech requires periodic repetition, rephrasing, or provision of a cue, Level 6 – spontaneous production of speech is intelligible in and out of context, but the production is sometimes distorted, Level 7 – production of speech is normal in all situations.
Pseudohypocusis is the intentional, conscious act of feigning a hearing loss as a form of deception. Other terms include non-organic, functional, malingering.
Men are more apt to fake a loss if there is financial gain involved.
Women will fake if pressured.
Kids use it as an attention getting device, especially prepubescent females.
Signs of Pseudohypocusis
Patient often indicates a very specific incident that caused the “loss”
There is something to be gained financially from the “loss” (often referred by a lawyer)
Very exaggerated lip reading, movements, etc.
Test/retest will be all over the place, not within the acceptable 10 dB range.
Acoustic reflexes will be present.
Stenger: test for unilateral loss. Have to have a 20 dB difference between the ears.
MADGE: minimal ascending descending gap evaluation. Start at 0 or -10, ascent until threshold at each frequency. Let patient rest, then start at very high level and descend to get thresholds at each frequency. Fakers will have a big difference between thresholds.
Delayed pure tone and speech feedback: fakers will get tripped up with delayed tones and speech feedback, but if there is a true loss it wouldn’t bother them.
Lombard Test: masking noise in the “bad” ear. Have them repeat words. Fakers voice will get louder to compensate for noise.